cardiovascular drugs (2023)

  1. recently updated
  2. Save as PDF
  • ID of the page
  • \( \newcommand{\vecs}[1]{\overset { \scriptstyle \rightharpoonup} {\mathbf{#1}}}\) \( \newcommand{\vecd}[1]{\overset{-\!- \!\rightharpoonup}{\vphantom{a}\smash{#1}}} \)\(\newcommand{\id}{\mathrm{id}}\) \( \newcommand{\Span}{\mathrm{ span}}\) \( \newcommand{\kernel}{\mathrm{null}\,}\) \( \newcommand{\range}{\mathrm{range}\,}\) \( \newcommand{\RealPart }{\mathrm{Re}}\) \( \newcommand{\ImaginaryPart}{\mathrm{Im}}\) \( \newcommand{\Argument}{\mathrm{Arg}}\) \( \newcommand{\ norma}[1]{\| #1 \|}\) \( \newcommand{\inner}[2]{\langle #1, #2 \rangle}\) \( \newcommand{\Span}{\mathrm {span}}\) \(\newcommand{\id}{\mathrm{id}}\) \( \newcommand{\Span}{\mathrm{span}}\) \( \newcommand{\kernel}{\ mathrm{null}\,}\) \( \newcommand{\range}{\mathrm{range}\,}\) \( \newcommand{\RealPart}{\mathrm{Re}}\) \( \newcommand{ \ImaginaryPart}{\mathrm{Im}}\) \( \newcommand{\Argumento}{\mathrm{Arg}}\) \( \newcommand{\norm}[1]{\| #1 \|}\) \( \newcommand{\inner}[2]{\langle #1, #2 \rangle}\) \( \newcommand{\Span}{\mathrm{span}}\)\(\newcommand{\AA}{ \unicode[.8,0]{x212B}}\)

    Cardiovascular diseases are the leading cause of death in industrialized countries. Like cancer, which is the second leading cause of death, the incidence of cardiovascular disease increases with age, accounting for about two-thirds of all deaths in people over age 75. Although some diseases primarily affect the heart and others the vascular system, they cannot be separated from each other. This obvious interdependence creates a unified imperative. One of the main diseases, atherosclerosis, attacks and ends up damaging the heart, kidneys and other organs.

    A. Antihypertensives

    Hypertension is generally defined as an increase in systolic and/or arterial blood pressure, and a value of 140/90 torr is generally accepted as the upper limit of normal blood pressure. Some risk factors (eg, hypercholesterolemia, diabetes, smoking, and family history of vascular disease) in combination with hypertension predispose to atherosclerosis and, consequently, to cardiovascular morbidity. Patient populations with sustained diastolic blood pressure in the range of 105 to 129 Torr clearly benefit from effective blood pressure reduction. The benefits of antihypertensive treatment are the prevention of accelerated or malignant hypertension, a lower incidence of hypertensive renal failure, and a reduction in the incidence of hemorrhagic stroke and heart failure. Only recently has it been shown that aggressive treatment of patients with mild diastolic hypertension can significantly reduce the incidence of myocardial infarction.

    Sympathetic function inhibition

    B- blockers

    Because they were introduced in the 1960s.BAdrenergic blockers have become the most commonly used drugs in cardiovascular disease. The first was propranololB-blocker to come into wide clinical use and remains the most important of these compounds. It is a very potent non-selective adrenergic blocking agent that has no intrinsic sympathomimetic activity. However, due to its ability to blockBreceptors on bronchial smooth muscle and skeletal muscle, propranolol impairs epinephrine-induced bronchodilation and glycogenolysis that commonly occurs during hypoglycemia. Therefore, the drug is generally not used in people with asthma and should be used with caution in diabetics receiving insulin. Thus began the searchB-blockers that are cardioselective and many drugs have already been developed that show some degree of specificity forB1-adrenergic receptors. Metaprolol is the prototype of these more specific drugs.

    cardiovascular drugs (1)

    a lot of pharmacologyB-blockers can be inferred from the knowledge of the functions supported by the receptors involved and the physiological conditions in which they are activated. Thus, β-receptor blockade has little effect on the normal heart of a patient at complete rest, but can have profound effects when sympathetic control of the heart is high, as during exercise.B- blockers reduce heart rate and cardiac output, prolong mechanical contraction and slightly lower blood pressure in people at rest. As a result of compensatory sympathetic reflexes, peripheral resistance increases and blood flow to all tissues except the brain is reduced. Some of these drugs also have direct effects on cell membranes, which are commonly described as membrane stabilizers and local anesthetics. The local anesthetic effect of propranolol is approximately the same as that of lidocaine.

    B-blockers are effective antihypertensive drugs. Chronic treatment of hypertensive patients with beta-adrenergic blockers results in a slowly progressive decrease in blood pressure. Several mechanisms have been proposed for the effectiveness of β-blockers in the treatment of hypertension. Decreased cardiac output occurs rapidly after administration of beta-blockers. However, the hypotensive effectB-blockers don't spawn as fast. The release of renin from the perilingual apparatus is stimulated by adrenergic agonists and this action is blocked by drugs such as propranolol. Also, BBeta-adrenergic agonists are known to slightly increase the release of norepinephrine from adrenergic nerve endings, resulting in vasoconstriction.BBlockers block this effect, and this impairment of norepinephrine release following sympathetic nerve stimulation may contribute to the drugs' antihypertensive effect.

    A- blockers

    Alpha-adrenergic blocking agents are present in most blood vessels, especially resistance vessels. Since their stimulation leads to constriction and therefore an increase in blood pressure, it is understandable that blocking this stimulation leads to a decrease in blood pressure. Phenoxybenzamine binds covalently to the α receptor and forms an irreversible blockade. Phentolamine and tolazoline reversibly bind and competitively antagonize the action of sympathomimetic amines.

    cardiovascular drugs (2)


    serpentinowa rauwofiaIt is a climbing shrub native to India and neighboring countries. In 1954, it was reported that rauwolfia or reserpine was useful in the treatment of psychotic patients because it acts centrally, producing a characteristic sedation and a state of indifference to environmental stimuli; phenothiazine-like effects (discussed in Psychoactive Drugs). The subsequent discovery of the ability of rauwolfia alkaloids and related compounds to remove biogenic amines from storage sites in the body initiated many studies aimed at elucidating the interactions between these amines and reserpine. There are many rauwolfia alkaloids with a complex structure. The structure of reserpine is as follows:

    cardiovascular drugs (3)

    It is clear that reserpine interferes with intracellular storage of catecholamines, but the amounts of reserpine in tissues are too small to assume a stoichiometric shift. Reserpine antagonizes norepinephrine uptake by isolated chromaffin granules by ATP-Mg inhibition2+Mechanism of uptake dependent on the granular membrane. The drug also binds to the alveolar membranes for several days, which is responsible for the irreversibility of the process.

    (Video) Pharmacology - CHF Heart failure & ANTIHYPERTENSIVES made easy - for Registered Nurse Rn & PN NCLEX

    Reserpine depletes catecholamine stores in many organs, including the brain and adrenal medulla, and most of its pharmacological effects are attributed to this action. As reuptake is inhibited, rather than catecholamine release, the existing pool must be completely depleted before antihypertensive effects become apparent. Even at relatively high doses, reserpine produces a transient sympathomimetic effect followed by a slowly progressive drop in blood pressure, often accompanied by bradycardia. At normal doses, reduced levels of catecholamines can be measured within one hour of reserpine administration, and depletion is maximal after 24 hours. Most catecholamines are deaminated within neurons, and the pharmacologic effects of the released mediator are minimal unless MAOIs have been inhibited.

    The reserpine-induced decrease in norepinephrine synthesis is a blockade of dopamine uptake into storage granules containing the enzyme dopamine.B-hydroxylase (see norepinephrine synthesis). Furthermore, increasing the concentration of free catecholamines probably inhibits tyrosine hydroxylase, as norepinephrine competes with the cofactor pterin for the enzyme.

    Hypersensitivity to catecholamines is observed after chronic use of reserpine. The site of change is presumably postjunctional and may be due to changes in adrenergic receptors. Such adaptive change is usually the result of chronic transmitter deprivation.

    Reserpine is used as an effective antihypertensive, especially when combined with other agents such as diuretics. Its low cost, once-daily administration, and minimal change in effect when adherence is inconsistent make it useful as a long-term treatment for patients with uncomplicated mild hypertension. However, reserpine causes mental depression in 25% of patients.


    A diuretic is a substance that increases the rate of urine excretion, as the name suggests. Most diuretics also increase urinary excretion of solutes, especially sodium and chloride. In fact, most clinically used diuretics work by reducing the rate of sodium reabsorption from the nephron tubules, which in turn causes nature, and this, in turn, causes diuresis. The most common clinical use of diuretics is to reduce the volume of extracellular fluids, mainly in diseases associated with edema and hypertension.

    carbonic anhydrase inhibitors

    Shortly after the introduction of sulfonamides as antibacterial agents in the 1930s, changes in patients' electrolyte balance and systemic acidosis with urine alkalinization due to increased HCO3-excretion. Proposals by several scientists have established that inhibition of the enzyme carbonic anhydrase (CA) is responsible for the electrolyte imbalances produced. Since the antibacterial sulfonamides were relatively weak inhibitors, a successful search for a more potent CA inhibition was initiated. Acetazolamide became the first effective drug introduced into clinical use.

    Of the large number of sulfonamides that have been synthesized and tested, acetazolamide has been studied most extensively as a carbonic anhydrase inhibitor. Other drugs in this class available in the US include dichlorphenamide and methazolamide. There, the structural formulas are as follows:

    cardiovascular drugs (4)

    Mechanism of action.The kidneys control the body's acid-base balance by excreting acidic or alkaline urine. The general mechanism by which the kidneys achieve this is as follows: Large numbers of bicarbonate ions are continually filtered into the renal tubules, and if they are excreted in the urine, this removes alkali from the blood. On the other hand, large amounts of hydrogen ions are also secreted into the lumen of the tubules by the tubular epithelial cells, thus removing acids from the blood.

    Bicarbonate ions enter the lumen of the renal nephron tubules along with the glomerular filtrate. Bicarbonate ions do not easily penetrate the luminal membranes of renal tubular cells; therefore, the bicarbonate ions that are filtered by the glomeruli cannot be directly reabsorbed. Instead, bicarbonate is reabsorbed in a special process where it first combines with hydrogen ions to form H2SWINDLER3, which eventually becomes CO2I H2O.

    \[\ce{ H^{+} + HCO3 <=> H2CO3 <=> CO2 + H2O}\]

    This reabsorption of bicarbonate ions is initiated by a reaction in the tubules between bicarbonate ions filtered in the glomeruli and hydrogen ions secreted by the tubular cells. H2SWINDLER3is formed and then dissociates into CO2I H2CO2can move easily through the tubular membrane; therefore, it immediately diffuses into the tube cell where it recombines with the H2O, under the influence of carbonic anhydrase, to produce a new H2SWINDLER3molecule. este H2SWINDLER3in turn dissociates to form a bicarbonate ion and a hydrogen ion. Hydrogen ions are secreted from the cell into the lumen of the tube by the sodium-hydrogen pump in exchange for sodium. Bicarbonate ions along with said Na+ then enter the peritubular blood supply. The hydrogen ion now in the lumen of the tube combines with another bicarbonate ion to form H2SWINDLER3, which is then dehydrated again in CO2, which re-enters the tube cell. The net result is reabsorption of most of the bicarbonate. Some of these concepts can be seen here in an animated nephron (you need the Shockwave plugin to see this).cheered up

    The mechanism of hydrogen bonds, which act competitively, explains the effects of carbonic anhydrase inhibitors similar to acetazolamide, which have diuretic properties. Carbonic acid is a normal substrate that fits into the cavity and forms complexes with the enzyme carbonic anhydrase. This complex is strongly stabilized by four hydrogen bonds (see figure below).

    cardiovascular drugs (5)

    (Video) Heart Failure | Pharmacology (ACE, ARBs, Beta Blockers, Digoxin, Diuretics)

    Acetazolamide-like drugs that fit into the enzyme cavity also bind efficiently, presumably to the same four regions via hydrogen bonds (see figure below).

    cardiovascular drugs (6)

    Thus, these sulfonamides competitively prevent the binding of carbonic acid at this site, which inhibits NaHCO reabsorption.3I H20. More than 99% of enzyme activity in the kidneys must be inhibited before physiological effects become apparent.

    Urinary volume increases rapidly after administration of acetazolamide. Urinary excretion of bicarbonate and related cations, primarily sodium (also potassium) and the normally acidic pH becomes alkaline. As a result, the concentration of bicarbonate in the extracellular fluid is reduced and metabolic acidosis occurs. The concentration of chloride in the urine decreases.

    The presence of carbonic anhydrase in many intraocular structures, including the ciliary processes, and the high concentration of bicarbonate in aqueous humor have drawn attention to the role that this enzyme may play in aqueous humor secretion. acetazolamide reduces the rate of aqueous humor formation; intraocular pressure in patients with glaucoma is correspondingly reduced.


    Thiazines and related compounds are the most commonly used antihypertensive drugs in the United States. They were synthesized as an extension of research on carbonic anhydrase inhibitors. Thiazides act directly on the kidneys to increase excretion of sodium chloride and its associated water volume. In addition, many of these drugs act as carbonic anhydrase inhibitors. At the molecular level, it is not known how benzothiadiazines inhibit sodium chloride reuptake.

    cardiovascular drugs (7)

    B. Antianginal drugs: coronary vasodilators

    Angina pectoris, or ischemic heart disease, is the name given to symptomatic and uncomfortable pain resulting from myocardial ischemia. Simply put, it arises when the oxygen demand of the myocardial tissues exceeds the circulatory supply. When local anemia due to obstruction occurs, biochemical changes are inevitable. Waste products accumulate in the area, contractility decreases, and sympathetic neurons release NEs. The end result is pain. The underlying pathology of typical angina pectoris is usually advanced atherosclerosis and coronary stenosis resulting in local hypoxia. Episodes are precipitated by emotional stress or exercise but usually resolve quickly with rest or nitroglycerin. In contrast, variant angina is caused by coronary vasoconstriction and may or may not be associated with severe atherosclerosis. Patients with variant angina have chest pain at rest.

    Until recently, many drugs used to prevent angina attacks were no more effective than a placebo. In truth. placebo has been reported to improve symptoms in up to 50% of patients with angina pectoris. However, it has been known for over a century that nitroglycerin is useful in preventing or relieving acute angina attacks. recent effectivenessB-Adrenergic antagonists have been established for long-term prophylaxis of typical angina pectoris. Furthermore, calcium channel blockers appear to be effective in the treatment of vasospastic angina pectoris. Although antianginal drugs provide only symptomatic treatment, administration of these drugs appears to reduce the incidence of sudden death related to ischemia and myocardial infarction.

    organic nitrates

    Organic nitrates and nitrites are smooth muscle dilators in arteries and veins. The dilation of the veins causes a decrease in the end-diastolic pressure of the left and right ventricles, which is greater than the decrease in blood pressure in the circulatory system. Net systemic vascular resistance generally remains relatively unchanged; heart rate remains unchanged or slightly increased; and pulmonary vascular resistance is continuously reduced. These drugs correct myocardial underoxygenation by increasing oxygen supply to the ischemic myocardium by direct coronary vasodilation and by reducing oxygen demand by reducing the work of the heart. The latter is due to the drop in pressure in the vessels, allowing the heart to pump blood more easily.

    Glycerin trinitrate

    Glycerol trinitrate or nitroglycerin is a thick, sweet-smelling oil that is highly explosive. The most used pharmaceutical form of nitroglycerin was the sublingual tablet. Oral absorption is rapid, offering almost immediate relief, lasting long enough (<30 min) for emergencies. However, due to the valuable properties of nitroglycerin, which are now known to have effects on angina pectoris, continuous blood levels of the drug are desirable. Therefore, several innovative dosage forms are being developed. As nitroglycerin is effectively absorbed through the skin, this has led to the introduction of nitroglycerin skin patches. These patches contain the drug in a form that causes it to be released continuously.

    cardiovascular drugs (8)

    (Video) Hypertension/Angina Medications - Pharmacology - Cardiovascular | @LevelUpRN

    Mechanism of action

    Nitric oxide (NO) has been shown to be an important transmitter in many signal transduction processes. This free radical gas is naturally produced endogenously from arginine in a complete reaction catalyzed by nitric oxide synthetase (NOS).

    cardiovascular drugs (9)

    Nitroglycerin, organic nitrites and nitrates also lead to the formation of the reactive free radical NO and is the basis of its mechanism of action. However, the exact enzyme that converts these drugs into NO is not known.

    Nitric oxide freely diffuses across membranes but has a short lifetime of less than a few seconds because it is highly reactive. Nitric oxide then activates the heme prosthetic group in the enzyme guanylate cyclase in the cell membrane. As a result, the heme molecule acts as an extremely sensitive NO detector. Part of the enzyme enters the cell and causes the formation of cyclic guanosine monophosphate (cGMP), the so-called secondary relay. cGMP has multiple effects, one of which is to alter the degree of phosphorylation of various enzymes that indirectly inhibit contraction. In particular, the pump that pumps calcium ions from the sarcoplasm to the sarcoplasmic reticulum is turned on, as is the cell membrane pump that pumps calcium ions out of the cell itself; these effects reduce the intracellular concentration of calcium ions, thereby inhibiting contraction.


    Viagra, an experimental heart drug with a wonderful side effect. more about viagra chemistry

    C. Daedalus

    Digitalis is a dried foxglove leaf,Digitalis purpurea. The seeds and leaves of many other species also contain heart active ingredients. The two digitalis molecules responsible for its pharmacological activity are digoxigenin and digitoxigenin. As you can see in the structures below, these genins are chemically related to sex hormones and the adrenal cortex.

    cardiovascular drugs (10)

    Digitalis has a powerful effect on the heart muscle that is unrivaled in the treatment of heart failure. It is also used to slow the ventricular rate in the presence of atrial fibrillation and flutter. The main pharmacodynamic property of digitalis is its ability to increase the force of myocardial contraction. Beneficial effect of the drug in patients with heart failure - increased cardiac output; reduced heart size. venous pressure and blood volume; diuresis and relief of edema - all are explained by increased contractile strength, positive inotropic effect.

    The most important component of the positive inotropic effect of digitalis is the direct inhibition of K+-activated membrane-bound ATPase, leading to an increase in intracellular [Ca+]. It seems clear that digitalis at therapeutic concentrations has no direct effect on contractile proteins or their interactions. Furthermore, it seems unlikely that the positive inotropic effect of digitalis is due to any action of cellular mechanisms that provide chemical energy for contraction. The hydrolysis of ATP by the Na+, K+-ATPase provides energy for the so-called sodium-potassium pump - a system in the sarcolemma of cardiac fibers that actively squeezes out sodium and transports potassium to the fibers. Digitalis drugs bind specifically to Na+, K+-ATPase, inhibit their enzymatic activity and impair the active transport of these two monovalent cations. As a result, there is a gradual increase in intracellular [Na+] and a gradual decrease in internal [K+]. These changes are minimal at therapeutic drug concentrations. This is believed to be decisively related to the positive inotropic effect of digitalis. This is because in cardiac fibers, intracellular Ca2+is exchanged for extracellular Na+ by another transmembrane pump. When intrinsic [Na+] levels increase due to inhibition of the Na+,K+ pump by digitalis, extracellular Na+ is exchanged for intracellular Ca2+is reduced and the inner [Ca2+] increases. The likely consequence of this is an increased supply of Ca2+in the sarcoplasmic reticulum and with each action potential, greater release of Ca2+activate the contractile apparatus.

    The interactions of Na+, K+-ATPase with their various substrates are complex. Thus, binding affinities for ATP, cofactor MG2+, Na+, K+ and digitalis are important for the overall effect. It is now hypothesized that the digitalis receptor is one or more Na+, K+-ATPase conformations that occur during operation of the ion pump, possibly in a state where the drug helps to stabilize one of the intermediate states of the enzyme.

    Evidence suggests that the entire glycoside molecule is involved in the proposed drug-receptor interaction. The steric relationship of the lactone ring to the steroid nucleus is absolute. Double bonding is also critical because saturation results in almost complete loss of activity. The necessary stereochemical positions of the C and D rings relative to each other (cis) and A and B (cis) and the OH configuration of C-14 (between the C and D rings) were established. The figure below is a very simplified version of the proposed interaction of the lactone side chain with such a digitalis receptor.

    cardiovascular drugs (11)

    The polarized carbonyl group, together with the electron-rich oxygen, is believed to bond hydrogen to a hydroxyl group on the surface of the enzyme, possibly to a serine residue, and the carbon atom attached to the steroid nucleus is attracted to the nucleus. electron dense. site in a secondary location.More information about Digitalis

    (Video) Digoxin Nursing Pharmacology NCLEX (Cardiac Glycosides)

    D. Anticoagulants

    By all accounts, blood is the most chemically complex tissue in the body. In addition to a multitude of cells and platelets, it contains inorganic ions, various plasma proteins, hormones, lipids, vitamins, a wide variety of enzymes, breakdown products of nucleic acids, a large number of unknown types of chemical substances absorbed from the environment. in various stages of development. metabolism, gases and water. Among them is a group of more than a dozen chemical agents that, when properly activated, will make the blood clot.

    Hemostasis is the spontaneous cessation of bleeding from damaged vessels. Precapillary vessels shrink immediately after being cut. Within seconds, thrombocytes attach to the exposed collagen of the damaged vessel. Platelets also stick together and form a sticky mass. This platelet plug can stop bleeding quickly, but it must be reinforced with fibrin for long-term effectiveness. This strengthening is initiated by local stimulation of the clotting process by the exposed collagen of the severed vessel and the released contents and platelet membranes. The two blood clotting pathways are shown in the figure below. Activation of circulating clotting factors depends on vitamin K.

    cardiovascular drugs (12)

    Thrombogenesis is the altered state of hemostasis. An intravascular thrombus is the result of a pathological disturbance of hemostasis. Arterial thrombus is initiated by the adhesion and release of circulating platelets to the vessel wall. This initial adhesion and release of adenosine diphosphate (ADP) from platelets is followed by platelet aggregation. The thrombus enlarges to occlusal size in areas of slower arterial blood flow. A platelet plug formed only by platelet interaction is unstable. After initial aggregation and viscous metamorphosis of platelets, fibrin becomes an important component of the thrombus. Thrombin is produced by activating the blood clotting reaction at the site of platelet aggregation. This thrombin further stimulates platelet aggregation, not only inducing the release of the ADP molecule from platelets, but also stimulating the synthesis of prostaglandins that are more potent than ADP.


    The first orally active anticoagulant, dicumerol, which is a molecule composed of two 4-hydroxy coumarin moieties connected at position 3 by a CH2 bridge, was isolated from decomposed yellow sweet clover. It was discovered and identified due to the hemorrhagic death of cattle consuming this improperly stored feed in the early 1920s (sweet clover disease). This followed the demonstration that oral administration of the compound prolonged clotting time and reduced the incidence of postoperative intravascular thrombus formation.

    cardiovascular drugs (13)

    Oral anticoagulants are vitamin K antagonists. Their administration to humans or other animals leads to the appearance of precursors of four vitamin K-dependent clotting factors in plasma and liver. These precursor proteins are biologically inactive in clotting assays. The prothrombin precursor protein can be non-physiologically activated to thrombin by snake venom, demonstrating that the part of the molecule required for this activity is intact. However, prothrombin and other precursor proteins cannot bind divalent cations such as calcium and therefore cannot interact with membranes containing phospholipids, which are their normal activation sites. This was puzzling for a while because abnormal prothrombin has the same number of amino acid residues and gives the same amino acid analysis after acid hydrolysis as normal prothrombin. NMR studies have shown that normal prothrombin containsG-carboxyglutamate (see figure below), a previously unknown residue. The vitamin K-sensitive step in the synthesis of clotting factors is the carboxylation of ten or more glutamic acid residues at the amino terminus of the precursor protein to formG-carboxyglutamate. These amino acid residues are much more potent calcium chelators than glutamate. Binding of Ca2+ by prothrombin anchors it to platelet-derived phospholipid membranes after damage. The functional significance of prothrombin binding to phospholipid surfaces is that it brings prothrombin closer to the two proteins that mediate its conversion to thrombin, factor Xa and factor V. The amino-terminal fragment of prothrombin, which contains Ca2+ binding sites, is released in this step of activation. The thrombin thus released from the surface of the phospholipids can then activate plasma fibrinogen.

    cardiovascular drugs (14)

    In liver microsomes, the reduction of vitamin K to the form of hydroquinone (vitamin KH2) precedes the bicarbonate-dependent carboxylation of the precursor prothrombin, decarboxyprothrombin, to prothrombin (see figure below). This carboxylase activity for prothrombin synthesis is related to the epoxidase activity for vitamin KH2, which oxidizes the vitamin to vitamin K epoxide (KO). Epoxide reductase, which requires NADH, converts vitamin K epoxide back to vitamin KH2. This reaction is the site of action for coumarins and the site of genetic resistance to coumarins, which is also characterized by an increased requirement for vitamin K. Therefore, it is the recycling of the vitamin into its reduced active cofactor that ultimately leads to decreased thrombin levels. The vitamin K analogue chloro-K1 (in which the 2-methyl group of vitamin K1 is replaced by a chloro group) directly inhibits the reaction of carboxylase and epoxidase, which are not sensitive to coumarins.

    cardiovascular drugs (15)

    Vitamin K is reduced to the form of hydroquinone (KH2). Gradual oxidation to vitamin K epoxide (KO) is coupled to protein carboxylation, where decarboxyprothrombin is converted to prothrombin by carboxylation of glutamate residues to g-carboxyglutamate. Enzymatic reduction of epoxide with NADH as a cofactor regenerates vitamin KH2. Vitamin KH Oxidation2. Vitamin K oxidation is inhibited by the chlorine analogue of vitamin K epoxide, which is a coumarin-sensitive step.

    Dicoumerol, the prototype coumarin drug, is relatively low potency, with a slow onset of up to 5 days for maximum activity and hypoprothrombinemia. The anticoagulant effect may persist for more than 1 week after discontinuing the drug. Although excessive doses can be treated with vitamin K1, clinical correction of anticoagulation, especially downwards, is difficult. Warfarin has become the most widely used coumarin drug. It is the strongest, and many patients stick to just 5 mg a day.

    Warfarin was initially introduced as a rodenticide because it was thought to be too dangerous for humans. It is still used for pest control. The drug, in the form of sugared pills, causes the death of rats by internal bleeding. Warfarin resistant rats were reported in London in the early 1960's. They were called "super rats". A few years later, this phenomenon appeared in humans. It has been shown to be an autosomal dominant trait. A person with this trait requires a 20-fold increase in drug dose to achieve anticoagulation - easily fatal for healthy patients. Explanations for this unusual phenomenon have been proposed. One is that a tissue protein that regulates the synthesis of one or more clotting factors has been genetically altered. Another is a mutation in the daphorase enzyme that makes it less susceptible to inhibition by coumarin drugs.


    1. What factors affect the heart's supply and demand for O2?
    2. What are the symptoms and etiology of angina pectoris?
    3. Both nitrates and beta-blockers have antianginal properties. Compare and compare the pharmacological effects of these two classes of compounds.
    4. What are the sites of action of nitrates?
    5. When prescribing nitrates, what would you advise the patient about side effects?
    6. What are the benefits of calcium channel blockers in the treatment of angina pectoris? What is its mechanism of action? What are the contraindications for its use?
    7. What are the two main goals of pharmacotherapy for angina pectoris?
    8. What is the mechanism of action of nitroglycerin?
    (Video) Hypertension medications that affect the RAAS system - Pharmacology - Cardiovascular | @LevelUpRN

    Collaborators and Assignments


    Cardiovascular drugs? ›

    Examples of agents in this class include chlorothiazide, amiloride, furosemide, bumetanide, indapamide and spironolactone. Vasodilators - These drugs relax the blood vessels and cause blood pressure to fall. They are useful in the treatment of high blood pressure, heart failure, angina and heart attacks.

    What are 4 examples of cardiovascular drugs? ›

    There are lots of different medicines used to treat diseases of the heart, but they all belong to a few main groups, including:
    • ACE inhibitors like ramipril.
    • angiotensin-II antagonists like losartan.
    • anti-arrhythmic medicines like amiodarone.
    • anticoagulant medicines like warfarin.
    • anti-platelet medicines like aspirin.
    Mar 1, 2023

    What are the top 10 heart medications? ›

    What are the Most Common Heart Medications?
    • Aspirin to prevent blood clots. ...
    • ACE inhibitors or ARBs to treat high blood pressure and other conditions. ...
    • Antiarrhythmics to treat arrythmias. ...
    • Anticoagulants (blood thinners) to prevent blood clots. ...
    • Beta blockers to help your heart work better.
    Jun 3, 2021

    How are cardiovascular drugs classified? ›

    They can be categorized into: 1) Angiotensin – converting enzyme inhibitors, that reduce the production of angiotensin-II and -III, chemicals that cause arterioles to constrict; 2) sympathetic nervous system depressants including vasodilators and calcium channel blockers, each of which cause dilatation of blood vessels ...

    What are cardioactive drugs used for? ›

    Vasodilators relax the blood vessels and are used to treat hypertension and angina. Digitalis – This cardio-active drug is a steroid that activates the cardiac muscle and is used to treat heart failure, arrhythmia and atrial fibrillation.

    What are the 5 cardiac emergency drugs? ›

    • Adrenaline. This is the first drug given in all causes of cardiac arrest and should be readily available in all clinical areas. ...
    • Amiodarone. ...
    • Lidocaine. ...
    • Atropine. ...
    • Additional drugs. ...
    • Calcium chloride. ...
    • Magnesium sulphate. ...
    • Miscellaneous drugs.
    Jun 6, 2006

    What medication relaxes the heart? ›

    Beta-Blockers to Slow Your Heart Rate
    • Atenolol (Tenormin)
    • Bisoprolol (Zebeta, Ziac)
    • Carvedilol (Coreg)
    • Metoprolol (Lopressor, Toprol)
    • Propranolol (Inderal, Innopran)
    • Timolol (Blocadren, Istalol)
    Feb 20, 2023

    What drugs prevent heart attacks? ›

    Antiplatelets (Aspirin, ASA, acetylsalicylic acid, clopidogrel, dipyridamole, ticlopidine) Antiplatelets help stop dangerous blood clots from forming. This can reduce the risk of heart attack or stroke. Aspirin is the most common antiplatelet.

    What is the drug of first choice in heart failure? ›

    There are many different types of diuretic, but the most widely used for heart failure are furosemide (also called frusemide) and bumetanide.

    What medication dissolves plaque in arteries? ›

    Statins help lower low-density lipoprotein (LDL) cholesterol, also known as “bad” cholesterol, in the blood. They draw cholesterol out of plaque and stabilize plaque, Blaha says.

    Is Lipitor a cardiovascular drug? ›

    Doctors commonly prescribe Lipitor together with diet, weight loss and exercise to lower cholesterol and help stave off cardiovascular disease in people with multiple risk factors other than pre-existing coronary heart disease. The FDA approved Lipitor for this use based on clinical trials.

    What drugs increase blood flow? ›

    A list of common vasodilators includes:
    • ACE inhibitors such as benazepril (Lotensin®) or lisinopril (Prinivil®, Zestril®).
    • ARBs such as losartan (Cozaar®).
    • CCBs such as diltiazem (Cardizem®, Tiazac®).
    • Other direct vasodilators such as hydralazine (Apresoline®), minoxidil (Loniten®) or nitroglycerin (Nitrostat®).
    Jun 9, 2022

    What drug is used to speed up the heart? ›

    Epinephrine is a stimulant. It is given during cardiac arrest to make the heart beat. Other times, stimulants can cause unwanted side effects. For example, pseudoephedrine found in some cold medicines can increase the heart rate.

    What cardiac drug is used for tachycardia? ›

    Medicines for treating tachycardia

    Medicines used to slow the heart rate: Digitalis or Digoxin. Verapamil. Diltiazem (Cardizem®)

    What is the most toxic cardiac drug? ›

    The most well-known cause of cardiac toxicity is the chemotherapy drug doxorubicin (Adriamycin®). Doxorubicin is a type of chemotherapy drug called an anthracycline.

    What are the big four heart failure drugs? ›

    Thus, in clinical practice, patients without contraindications appear to gain most benefit from combined treatment with the 'fantastic four': an ARNI, a beta-blocker, an MRA, and an SGLT2 inhibitor (Figure 1).

    What are the 10 emergency drugs? ›

    List of Emergency Drugs and their Actions
    • Drug- Aspirin. Dose- 81 mg chewable tablet. ...
    • Drug- Adenosine. ADVERTISEMENT. ADVERTISEMENT. ...
    • Drug- Albuterol. Dose- ...
    • Drug- Amiodarone. Dose- ...
    • Drug- Atropine. Dose- ...
    • Drug- Calcium Chloride 10%** Dose- ...
    • Drug- Dexamethasone. Dose- ...
    • Drug- Dextrose. Dose-

    What are the new cardiac drugs? ›

    These drugs are creating quite a buzz in the cardiology community, and for good reason. For starters, there's the sheer number of them: Two drugs, Corlanor and Entresto, were approved by the FDA for heart failure patients. Two other medications – Praluent and Repatha – were approved for treating high cholesterol.

    What vitamin is good for heart health? ›

    • Vitamin D. There is some evidence that suggests there is a link between low blood levels of vitamin D and heart disease. ...
    • Folic Acid. Folic acid is a B vitamin. ...
    • Omega 3 Fatty Acid. ...
    • Magnesium.
    Feb 5, 2022

    What drugs make heart failure worse? ›

    But some can worsen heart failure, including:
    • Sulfonylureas like glyburide (Glynase) and glipizde (Glucotrol)
    • Thiazolidinediones (TZDs) like pioglitazone (Actos)
    • DPP-4 inhibitors like Onglyza (saxagliptin)
    Apr 21, 2021

    What is the miracle drug for heart failure? ›

    Empagliflozin is a vital new therapeutic option to reduce the risk of cardiovascular death and hospitalization for adults with heart failure with reduced ejection fraction.”

    What is the new wonder drug for heart failure? ›

    Today, the U.S. Food and Drug Administration approved Jardiance (empagliflozin) to reduce the risk of cardiovascular death and hospitalization for heart failure in adults.

    What drugs help the heart pump better? ›

    Digoxin to help increase the heart's pumping strength and slow the heart rate. Hydralazine and nitrates to open up arteries and help the heart muscle pump better. These drugs are mainly used by people who are unable to tolerate ACE inhibitors and angiotensin receptor blockers.

    What drug melts away fat in arteries? ›

    It was originally considered to treat breast cancer and diabetes, but a drug called Trodusquemine also seems to be extremely successful at clearing out fat in arteries.

    What drink can clean your arteries? ›

    Ginger, garlic and lemon detox drink – Boil ginger and garlic and strain. Squeeze the juice of one full lemon into it. This is strong detox drink to get rid of bad cholesterol and also flush out all toxins from the arteries.

    What is the best thing to unclog your arteries? ›

    Tips for lifestyle change
    • Eat a heart-healthy diet.
    • Make exercise a part of your routine. Aim for at least 150 to 300 minutes of moderate-intensity exercise, 75 to 150 minutes of vigorous exercise, or a combination of both.
    • Avoid smoking. ...
    • Limit your alcohol consumption.
    Sep 26, 2022

    What can I take instead of statins to lower cholesterol? ›

    7 cholesterol-lowering alternatives to statins
    • Fibrates. Mostly used for lowering triglyceride levels in patients whose levels are very high and could cause pancreatitis. ...
    • Plant stanols and sterols. ...
    • Cholestyramine and other bile acid-binding resins. ...
    • Niacin. ...
    • Policosanol. ...
    • Red yeast rice extract (RYRE) ...
    • Natural products.

    Why did they take Lipitor off the market? ›

    To help prevent heart disease, many doctors prescribe cholesterol-lowering medications called statins. Lipitor is a popular statin drug made by the pharmaceutical company Pfizer. Unfortunately, the drug has been linked to a number of health complications and has been the subject of a recall.

    What is the downside of statins? ›

    While statins are highly effective and safe for most people, they have been linked to muscle pain, digestive problems and mental fuzziness in some people. Rarely, they may cause liver damage.

    What opens blood vessels immediately? ›

    Vasodilators are medications that open (dilate) blood vessels. They affect the muscles in the walls of the arteries and veins, preventing the muscles from tightening and the walls from narrowing. As a result, blood flows more easily through the vessels.

    What relaxes blood vessels? ›

    Nitric oxide is an essential molecule required for overall health. As a vasodilator, nitric oxide signals the blood vessels to relax, allowing them to expand. This effect allows blood, nutrients, and oxygen to flow freely to every part of your body.

    What medications can cause poor circulation? ›

    Common Prescription Drugs Alter Blood's Flow
    Beta-blockersPropranolol, Carvedilol, Atenolol
    Calcium channel blockersNifedipine
    DecongestantsEphedrine, Sudafed
    Nonsteroidal anti-inflammatory drugs (NSAIDs)Ibuprofen (Motrin, Advil) Naproxen (Aleve)
    3 more rows
    Jul 1, 2014

    What is the safest blood pressure medication to take? ›

    Safe medications to use include methyldopa and potentially some diuretics and beta-blockers, including labetalol.

    What is the best and safest blood pressure medication? ›

    What Are the 4 Best Blood Pressure Drugs?
    • Thiazide diuretics. Used to help the body get rid of excess sodium (salt) and water and help control blood pressure. ...
    • ACE (angiotensin-converting enzyme) inhibitors. ...
    • Angiotensin receptor blockers (ARBs) ...
    • Calcium channel blockers.
    Jun 10, 2022

    What anxiety medication is good for heart palpitations? ›

    About propranolol

    It's used to treat heart problems, help with anxiety and prevent migraines. If you have a heart problem, you can take propranolol to: treat high blood pressure. treat conditions that cause an irregular heartbeat (arrhythmia), like atrial fibrillation.

    What is the emergency drug to high heart rate? ›

    Epinephrine may be used as a secondary measure if atropine and temporary heart pacing don't improve hemodynamic stability. Among other actions, epinephrine stimulates beta1 receptors, causing cardiac stimulation, which in turn increases the heart rate.

    What happens if you take nitro and you don't need it? ›

    Taking more of this drug than you need can lead to tolerance. This means that, over time, the drug may not work as well to treat your chest pain. Dissolve your dose under your tongue or in your cheek at the first sign of chest pain.

    What is a nitro pill for the heart? ›

    Nitroglycerin sublingual tablets are used to treat episodes of angina (chest pain) in people who have coronary artery disease (narrowing of the blood vessels that supply blood to the heart). It is also used just before activities that may cause episodes of angina in order to prevent the angina from occurring.

    What are 3 drugs that affect cardiac output? ›

    Inotropic agents such as milrinone, digoxin, dopamine, and dobutamine are used to increase the force of cardiac contractions.

    What drugs strengthen the heart muscle? ›

    Long term beta blockers help keep your heart failure from becoming worse. Over time, they may also help strengthen your heart. Common beta blockers used for heart failure include carvedilol (Coreg), bisoprolol (Zebeta), and metoprolol (Toprol).

    What is the number one drug for heart failure? ›

    Healthcare providers often prescribe ACE inhibitors and beta blockers as first-line treatments. These drugs are especially helpful for people who have a reduced ejection fraction. This means your left ventricle (the main pumping chamber of your heart) isn't pumping enough blood to your body.

    What drugs are toxic to the heart? ›

    Here are 10 examples of drugs that could precipitate or exacerbate heart failure.
    • NSAIDs. Nonsteroidal anti-inflammatory drugs (NSAIDs) can lead to major heart failure. ...
    • α1-blockers. ...
    • Antimalarial agents. ...
    • TNF-α inhibitors. ...
    • Albuterol. ...
    • Antineoplastic agents. ...
    • Antifungal medications. ...
    • Minoxidil.
    Feb 11, 2021

    What medication relaxes heart muscle? ›

    Nitroglycerin tablets, often taken for angina, are a vasodilator. These medications help relax the blood vessels and increase the supply of oxygen-rich blood to the heart, also reducing the heart's workload. Some other names for vasodilators are minoxidil and hydralazine.

    What drugs reduce heart blockage? ›

    • Blood-thinning medicines. ...
    • Statins. ...
    • Beta blockers. ...
    • Nitrates. ...
    • Angiotensin-converting enzyme (ACE) inhibitors. ...
    • Angiotensin-2 receptor blockers (ARBs) ...
    • Calcium channel blockers. ...
    • Diuretics.

    Can you rebuild a weak heart muscle? ›

    The heart is unable to regenerate heart muscle after a heart attack and lost cardiac muscle is replaced by scar tissue. Scar tissue does not contribute to cardiac contractile force and the remaining viable cardiac muscle is thus subject to a greater hemodynamic burden.


    1. Cardiovascular Medications
    2. Medication of Heart Failure – Cardiology | Lecturio
    (Lecturio Medical)
    3. Vasodilators & Antianginals - Pharmacology - Cardiovascular | @LevelUpRN
    (Level Up RN)
    4. Drugs That Affect the Cardiovascular System
    (Interactive Biology)
    5. Pharmacology | Cardiovascular Pharmacology | INBDE, NBDE Part II
    (Mental Dental)
    6. Cardiovascular Drugs in Respiratory Care (Quick Medical Overview)
    (Respiratory Therapy Zone)


    Top Articles
    Latest Posts
    Article information

    Author: Domingo Moore

    Last Updated: 10/24/2023

    Views: 6060

    Rating: 4.2 / 5 (53 voted)

    Reviews: 84% of readers found this page helpful

    Author information

    Name: Domingo Moore

    Birthday: 1997-05-20

    Address: 6485 Kohler Route, Antonioton, VT 77375-0299

    Phone: +3213869077934

    Job: Sales Analyst

    Hobby: Kayaking, Roller skating, Cabaret, Rugby, Homebrewing, Creative writing, amateur radio

    Introduction: My name is Domingo Moore, I am a attractive, gorgeous, funny, jolly, spotless, nice, fantastic person who loves writing and wants to share my knowledge and understanding with you.