Antihypertensive Drugs



Antihypertensive Drugs


Objectives


When you reach the end of this chapter, you will be able to do the following:



1 Briefly discuss the normal anatomy and physiology of the autonomic nervous system, including the events that take place within the sympathetic and parasympathetic divisions as related to long-term and short-term control of blood pressure.


2 Define hypertension.


3 Compare primary and secondary hypertension and their related manifestations.


4 Describe the protocol for treating hypertension as detailed in the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), including the rationale for its use.


5 List the criterion pressure values (in millimeters of mercury) for the hypertension categories of normal blood pressure, prehypertension, hypertension stage 1, and hypertension stage 2 as defined in JNC 7.


6 Using the most recent guidelines, compare the various drugs used in the pharmacologic management of hypertension with regard to mechanism of action, specific indications, adverse effects, toxic effects, cautions, drug interactions, contraindications, dosages, and routes of administration.


7 Discuss the rationale for the nonpharmacologic management of hypertension.


8 Develop a nursing care plan that includes all phases of the nursing process for patients receiving antihypertensive drugs.


Drug Profiles



Key Terms


Alpha1 blockers Drugs that primarily cause arterial and venous dilation through their action on peripheral sympathetic neurons. (p. 351)


Antihypertensive drugs Medications used to treat hypertension. (p. 349)


Cardiac output The amount of blood ejected from the left ventricle, measured in liters per minute. (p. 348)


Centrally acting adrenergic drugs Drugs that modify the function of the sympathetic nervous system in the brain by stimulating alpha2 receptors. Alpha2 receptors are inhibitory in nature and thus have a reverse sympathetic effect and cause decreased blood pressure. (p. 351)


Essential hypertension Elevated systemic arterial pressure for which no cause can be found; also called primary or idiopathic hypertension. (p. 349)


Hypertension A common, often asymptomatic disorder in which systolic blood pressure persistently exceeds 140 mm Hg and/or diastolic pressure exceeds 90 mm Hg. (p. 348)


Orthostatic hypotension A common adverse effect of adrenergic blocking drugs involving a sudden drop in blood pressure when a person changes position, especially when rising from a seated or horizontal position. (p. 352)


Prodrug A drug that is inactive in its given form, and which must be metabolized to its active form in the body, generally by the liver, to be effective. (p. 354)


Secondary hypertension High blood pressure caused by another disease such as renal, pulmonary, endocrine, or vascular disease. (p. 349)


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Anatomy, Physiology, and Pathophysiology Overview


Hypertension, defined as a persistent systolic pressure of greater than 140 mm Hg and/or a diastolic pressure greater than 90 mm Hg, affects approximately 50 million people in the United States and approximately 1 billion people worldwide, designating it as the most common disease state. As the population ages, the incidence of hypertension will continue to increase.


Hypertension is a major risk factor for coronary artery disease, cardiovascular disease (CVD), and death resulting from cardiovascular causes. It is the most important risk factor for stroke and heart failure, and it is also a major risk factor for renal failure and peripheral vascular disease. There is indisputable evidence regarding the relationship between blood pressure and risk of CVD; the higher the blood pressure, the greater the chance of developing CVD. For people 40 to 70 years of age, the risk of developing CVD doubles with each 20 mm Hg increase in systolic blood pressure or 10 mm Hg increase in diastolic pressure.


To gain insight into the treatment of hypertension, it is necessary to have a basic understanding of blood pressure. Blood pressure is determined by the product of cardiac output (4 to 8 L/min) and systemic vascular resistance (SVR). Cardiac output is the amount of blood that is ejected from the left ventricle and is measured in liters per minute. SVR is the resistance to blood flow that is determined by the diameter of the blood vessel and the vascular musculature. It is calculated by the blood pressure divided by the cardiac output. Numerous factors interact to regulate these two major variables and keep the blood pressure within normal limits. These are illustrated in Figure 22-1. These are the same factors that can cause high blood pressure, or hypertension, and are the targets of action of many of the antihypertensive drugs.



The diagnosis and treatment of hypertension have varied considerably over the years. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) was released in May 2003. This report provides treatment guidelines for hypertension assembled by two large expert panels based on a review of the latest clinical research publications on the disease. As with previous such reports, the development of JNC 7 was sponsored by the National Heart, Lung, and Blood Institute of the National Institutes of Health, the major governmental health research entity of the United States. The efforts of the Joint National Committee are intended to educate both health care professionals and the general public about the dangers of the disease and the importance of its treatment. The Eighth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 8) is scheduled to be published in 2012, and more information is available at www.nhlbi.nih.gov/guidelines/hypertension/jnc8/index.htm.


A new classification system for blood pressure was identified in the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 6) in 1997. The previously applied term mild hypertension did not adequately reflect the serious nature of the condition. This became evident when it was found that most of the morbidity and mortality actually occur in this group. In addition, whereas pre-JNC 6 reports had recommended a stepped-care pharmacologic approach to treating the illness, many practitioners believed that this approach no longer adequately reflected the current range of pharmacologic alternatives. In the JNC 6, individualized therapy was proposed as a more appropriate treatment strategy. This individualized approach continues to be emphasized in the JNC 7 and will most likely be continued in the JNC-8. Many patients will require two or more medications, even as initial therapy, depending on their individual cardiovascular risk factors such as obesity, diabetes, and family history.


The classification scheme used to categorize individual cases of hypertension has been simplified to the following four stages based on blood pressure measurements: normal, prehypertension, stage 1 hypertension, and stage 2 hypertension. (Refer to the JNC 7 at www.nhlbi.nih.gov/guidelines/hypertension.)


Hypertension can also be defined by its cause. When the specific cause of hypertension is unknown, it may be called essential hypertension (or idiopathic or primary hypertension). About 90% of cases of hypertension are of this type. Secondary hypertension accounts for the other 10%. Secondary hypertension is most commonly the result of another disease such as pheochromocytoma (adrenal tumor), preeclampsia of pregnancy (a pregnancy complication involving acute hypertension, among other symptoms), renal artery disease, sleep apnea, thyroid disease, or parathyroid disease. It may also result from the use of certain medications. If the cause of secondary hypertension can be eliminated, blood pressure usually returns to normal. If untreated, hypertension can cause damage to end organs such as the heart, brain, kidneys, and eyes.


The goal of antihypertensive therapy is the reduction of cardiovascular and renal morbidity and mortality. According to the JNC 7, the goal is to achieve a pressure of less than 140/90, which is associated with a decrease in CVD complications. In patients with hypertension and diabetes or renal disease, the goal is less than 130/80 mm Hg.


Fortunately, many significant advances have been made in both the ways to treat hypertension and in the understanding of the disease process. Large numbers of clinical trials have shown that adequately treating hypertension can prevent or delay CVD. Over the past 40 years, the development of new antihypertensive medications has had an enormous impact on the quality of life of people with hypertension. Drug therapy for hypertension first became available in the early 1950s with the introduction of ganglionic blocking drugs. However, unpleasant adverse effects and inconsistent therapeutic effects were common problems with these antihypertensive drugs. In 1953, the vasodilator hydralazine was introduced, and in 1958 the thiazide diuretics became available.


Since that time, several additional drug categories have been developed, including loop diuretics (also called potassium-wasting diuretics), potassium-sparing diuretics, beta blockers (beta receptor antagonists), angiotensin-converting enzyme (ACE) inhibitors, alpha1 antagonists, alpha2 agonists, angiotensin II receptor blockers (ARBs), calcium channel blockers (CCBs), vasodilators, and the newest class, the direct renin inhibitors. Although some of the medications mentioned in this chapter represent older classes of drugs, all are current therapeutic options listed in the treatment guidelines for hypertension published by the National Heart, Lung, and Blood Institute.


Pharmacology Overview


Drug therapy for hypertension needs to be individualized. Important considerations in planning drug therapy are whether the patient has multiple medical problems and what impact drug therapy will have on the patient’s quality of life. For example, sexual dysfunction in males is a common adverse effect of almost any antihypertensive drug and is the most common reason for nonadherence to drug therapy. Demographic factors, cultural implications, the ease of medication administration (e.g., a once-a-day dosing schedule or transdermal administration), and cost are other important considerations.


There are essentially seven main categories of pharmacologic drugs used to treat hypertension: diuretics, adrenergic drugs, vasodilators, angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), calcium channel blockers (CCBs), and direct renin inhibitors. All of these antihypertensive drugs (with the exception of diuretics) have some vasodilatory action. Those drugs in the vasodilator category are also called direct vasodilators. Drugs in any of these classes may be used either alone or in combination. The various categories and subcategories of antihypertensive drugs are listed in Box 22-1. The diuretics are discussed in detail in Chapter 28 and therefore are not covered in this chapter.



Review of Autonomic Neurotransmission


There are two divisions of the autonomic nervous system (ANS): the parasympathetic nervous system (PSNS) and sympathetic nervous system (SNS). Stimulation of the ANS is controlled by the neurotransmitters acetylcholine and norepinephrine. Receptors for both divisions of the ANS are located throughout the body in a variety of tissues. ANS physiology is reviewed in greater detail in the introductory sections of Chapters 18 to 21. Receptors located between the postganglionic fiber and the effector cells (i.e., the postganglionic receptor) are called the muscarinic or cholinergic receptors in the PSNS. Receptors in the SNS are called adrenergic or noradrenergic receptors (i.e., alpha or beta receptors). Physiologic activity at muscarinic receptors is stimulated by acetylcholine and cholinergic agonist drugs (see Chapter 20) and is inhibited by cholinergic antagonists (anticholinergic drugs; see Chapter 21). Similarly, physiologic activity at adrenergic receptors is stimulated by norepinephrine and epinephrine and adrenergic agonists (see Chapter 18) and inhibited by antiadrenergics (adrenergic blockers; i.e., alpha or beta receptor blockers) (see Chapter 19). Figure 22-2 shows how these various receptors are arranged in both the PSNS and SNS and indicates their corresponding neurotransmitters.



Adrenergic Drugs


Adrenergic drugs are a large group of antihypertensive drugs, as shown in Box 22-1. The alpha blockers and combined alpha/beta blockers were described in detail in Chapter 19. The adrenergic drugs discussed here exert their antihypertensive action at different sites.


Mechanism of Action and Drug Effects


Five specific drug subcategories are included in the adrenergic antihypertensive drugs as indicated in Box 22-1. Each of these subcategories of drugs can be described as having central action (in the brain) or peripheral action (at the heart and blood vessels). These drugs include the adrenergic neuron blockers (central and peripheral), the alpha2 receptor agonists (central), the alpha1 receptor blockers (peripheral), the beta receptor blockers (peripheral), and the combination alpha1 and beta receptor blockers (peripheral).


The centrally acting alpha2-adrenergic receptor agonists clonidine and methyldopa act by modifying the function of the SNS. Stimulation of the SNS leads to an increase in heart rate and force of contraction, the constriction of blood vessels, and the release of renin from the kidney, resulting in hypertension. The centrally acting adrenergic drugs work by stimulating the alpha2-adrenergic receptors in the brain. The alpha2-adrenergic receptors are unique in that receptor stimulation actually reduces sympathetic outflow, in this case from the central nervous system (CNS). This results in a lack of norepinephrine production, which reduces blood pressure. Stimulation of the alpha2-adrenergic receptors also affects the kidneys, reducing the activity of renin. Renin is the hormone and enzyme that converts the protein precursor angiotensinogen to the protein angiotensin I, the precursor of angiotensin II (AII), a potent vasoconstrictor that raises blood pressure.


In the periphery, the alpha1 blockers doxazosin, prazosin, and terazosin also modify the function of the SNS. They do so by blocking the alpha1-adrenergic receptors. When alpha1-adrenergic receptors are stimulated by circulating norepinephrine, they produce increased blood pressure. Thus, when these receptors are blocked, blood pressure is decreased. The drug effects of the alpha1 blockers are primarily related to their ability to dilate arteries and veins, which reduces peripheral vascular resistance and subsequently decreases blood pressure. This produces a marked decrease in the systemic and pulmonary venous pressures and an increase in cardiac output. The alpha1 blockers also increase urinary flow rates and decrease outflow obstruction by preventing smooth muscle contractions in the bladder neck and urethra. This can be beneficial in cases of benign prostatic hyperplasia (BPH).


The beta blockers also act in the periphery and include propranolol, metoprolol, and atenolol as well as several other drugs. These drugs are discussed in more detail in Chapters 23 and 25 because they are also used for angina and conduction problems. Their antihypertensive effects are related to their reduction of the heart rate through beta1 receptor blockade. Furthermore, beta blockers also cause a reduction in the secretion of the hormone renin (see section on ACE inhibitors), which in turn reduces both AII-mediated vasoconstriction and aldosterone-mediated volume expansion. Long-term use of beta blockers also reduces peripheral vascular resistance.


Two dual-action alpha1 and beta receptor blockers, labetalol and carvedilol, also act in the periphery at the heart and blood vessels. They have the dual antihypertensive effects of reduction in heart rate (beta1 receptor blockade) and vasodilation (alpha1 receptor blockade). Figure 22-3 illustrates the site and mechanism of action of the various antihypertensive drugs.



Indications


All of the drugs mentioned in this section are used primarily for the treatment of hypertension, either alone or in combination with other antihypertensive drugs. Various forms of glaucoma may also respond to treatment with some of these drugs. Clonidine also has several off-label uses (not approved by the U.S. Food and Drug Administration but still common in practice), including prophylaxis against migraine headaches and treatment of severe dysmenorrhea or menopausal flushing. It is also useful in the management of withdrawal symptoms in persons with opioid, nicotine, or alcohol dependency (see Chapter 17). The alpha1 blockers doxazosin, prazosin, and terazosin have been used to relieve the symptoms associated with BPH (see Chapter 19). They have also proved effective in the management of severe heart failure when used with cardiac glycosides (see Chapter 24) and diuretics (see Chapter 28).


Contraindications


Contraindications to the use of the adrenergic antihypertensive drugs include known drug allergy and may also include acute heart failure, concurrent use of monoamine oxidase inhibitors (see Chapter 16), severe mental depression, peptic ulcer, and severe liver or kidney disease. Asthma may also be a contraindication to the use of any noncardioselective beta blocker (e.g., carvedilol). The use of vasodilating drugs may also be contraindicated in cases of heart failure that is secondary to diastolic dysfunction.


Adverse Effects


The most common adverse effects of adrenergic drugs are bradycardia with reflex tachycardia, postural and postexercise hypotension, dry mouth, drowsiness, dizziness, depression, edema, constipation, and sexual dysfunction (e.g., impotence). Other effects include headaches, sleep disturbances, nausea, rash, and palpitations. There is a high incidence of orthostatic hypotension (a sudden drop in blood pressure during changes in position) in patients taking alpha blockers. Orthostatic hypotension is commonly referred to as postural hypotension. When the patient changes positions, a situation known as first-dose syncope, in which the hypotensive effect is severe enough to cause the patient to lose consciousness with even the first dose of medication, can occur. Educate the patient to change positions slowly.


In addition, the abrupt discontinuation of the centrally acting alpha2 receptor agonists can result in rebound hypertension, characterized by a sudden and very high elevation of blood pressure. This may also be true for other antihypertensive drug classes, especially beta blockers. Nonselective blocking drugs are also commonly associated with bronchoconstriction (due to unrestrained parasympathetic tone) as well as metabolic inhibition of glycogenolysis in the liver, which can lead to hypoglycemia. However, hyperglycemic episodes are also among the adverse effects reported for this drug class.


Any change in the dosing regimen for cardiovascular medications should be undertaken gradually and with appropriate patient monitoring and follow-up. Although the same is also true for most other classes of medications, abrupt dosage changes of cardiovascular medications, either up or down, can be especially hazardous for the patient. Some of these drugs can also cause disruptions in blood count as well as in serum electrolyte levels and renal function. Periodic monitoring of white blood cell count, serum potassium and sodium levels, and urinary protein levels is recommended.


Interactions


Adrenergic drugs can cause additive CNS depression when taken with alcohol, benzodiazepines, and opioids. Other drug interactions that can occur with selected adrenergic drugs are summarized in Table 22-1. This list is merely representative and is not exhaustive. Always keep a drug information handbook available to check in cases in which a specific drug interaction is suspected. Hospital pharmacists are also excellent resources.



Dosages


For dosage information on selected adrenergic antihypertensive drugs, see the table on p. 353.


Drug Profiles


Alpha2-Adrenergic Receptor Stimulators (Agonists)


Of the two alpha2 receptor agonists—clonidine and methyldopa—clonidine is by far the most commonly used and is the prototypical drug for this class. Methyldopa is commonly used to treat hypertension in pregnancy. However, these drugs are not typically prescribed as first-line antihypertensive drugs, because their use is associated with a high incidence of unwanted adverse effects such as orthostatic hypotension, fatigue, and dizziness. They may be used as adjunct drugs in the treatment of hypertension after other drugs have failed or may be used in conjunction with other antihypertensives such as diuretics.




♦ clonidine


Clonidine (Catapres) is used primarily for its ability to decrease blood pressure. It is also useful in the management of opioid withdrawal. It has a better safety profile than the other centrally acting adrenergics and has the advantage of being available in several dosage formulations, including both topical and oral preparations. When the patch dosage form is used, it is important to remove the old patch before applying a new one. Clonidine must not be discontinued abruptly, as this will lead to severe rebound hypertension. Its use is contraindicated in patients who have shown hypersensitivity reactions to it. Recommended dosages are given in the table on this page.



Alpha1 Blockers


The alpha1 blockers are doxazosin (Cardura), prazosin (Minipress), tamsulosin (Flomax), and terazosin (Hytrin). Their use is contraindicated in patients who have shown a hypersensitivity to them. They are classified as pregnancy category C drugs. They are available only as oral preparations. Tamsulosin is not used to control blood pressure but is indicated solely for symptomatic control of benign prostatic hyperplasia (BPH). This use is described further in Chapters 19 and 35.


doxazosin


Doxazosin (Cardura) is a commonly used alpha1 blocker. It reduces peripheral vascular resistance and blood pressure by dilating both arterial and venous blood vessels. It has been shown to be beneficial in the treatment of hypertension and the relief of the symptoms of obstructive BPH. It is available in immediate- and extended-release formulations. When the drug is released from the extended-release form, the matrix of the capsule is expelled in the stool. Educate patients that this will happen, and reassure that the active drug has been absorbed. Confusion over the presence of the capsule matrix could cause patients to take more than the prescribed dosage. Recommended dosages are given in the table on this page.



Dual-Action Alpha1 and Beta Receptor Blockers


carvedilol


Carvedilol (Coreg) is a widely used drug and is well tolerated by most patients. In addition to treatment of hypertension, it is also indicated for treatment of mild to moderate heart failure in conjunction with digoxin, diuretics, and ACE inhibitors. Its contraindications include known drug allergy, cardiogenic shock, severe bradycardia or heart failure, bronchospastic conditions such as asthma, and various cardiac problems involving the conduction system. For dosage information, see the table on this page.



Beta Receptor Blocker


nebivolol


Nebivolol (Bystolic) is the newest beta blocker, released in 2008. It is a beta1-selective beta blocker approved for use in hypertension. It is also used for the treatment of heart failure. Nebivolol is similar to other beta1-selective blockers; however, in addition to blocking beta1 receptors, it also produces an endothelium-derived nitric oxide–dependent vasodilatation, which results in a decrease in SVR. It is promoted as causing less sexual dysfunction. Like other beta blockers, it should not be stopped abruptly but must be tapered over 1 to 2 weeks. Dosing starts at 5 mg/day and may be increased at 2-week intervals to a maximum of 40 mg/day.


Angiotensin-Converting Enzyme (ACE) Inhibitors


The ACE inhibitors are a large group of antihypertensive drugs. Currently, there are ten ACE inhibitors available for clinical use. In addition, various combination drug products are available in which a thiazide diuretic or a calcium channel blocker (CCB) is combined with an ACE inhibitor. Combination products tend to increase adherence since the patient is taking fewer drugs. The available ACE inhibitors are captopril (Capoten), benazepril (Lotensin), enalapril (Vasotec), fosinopril (Monopril), lisinopril (Prinivil), moexipril (Univasc), perindopril (Aceon), quinapril (Accupril), ramipril (Altace), and trandolapril (Mavik). These drugs are very safe and efficacious and are often used as first-line drugs in the treatment of both heart failure and hypertension. Some of the available drug combinations and dosing schedules for the various drugs that make up this large class of antihypertensives are summarized in Table 22-2. The ACE inhibitors as a class are very similar to one another and differ in only a few of their chemical properties; however, there are some differences among them in their clinical properties.



Captopril has the shortest half-life and therefore must be dosed more frequently than any of the other ACE inhibitors. This may be an important drawback for patients with a history of nonadherence to their medication regimen. On the other hand, it may be best to start with a drug that has a short half-life in a patient who is critically ill, so that if problems arise they will be short-lived. Both captopril and enalapril can be dosed multiple times a day.


Captopril and lisinopril are the only two ACE inhibitors that are not prodrugs. A prodrug is a drug that is inactive in its administered form and must be metabolized to its active form in the body, generally by the liver, to be effective. This characteristic of captopril and lisinopril is an important advantage in treating a patient with liver dysfunction; all of the other ACE inhibitors are prodrugs, and their transformation to active form is dependent upon liver function to reveal the active drug.


Enalapril is the only ACE inhibitor that is available in a parenteral preparation. All of the newer ACE inhibitors, such as benazepril, fosinopril, lisinopril, quinapril, and ramipril, have long half-lives and long durations of action, which allows them to be given orally only once a day. A once-a-day medication regimen promotes better patient adherence.


All ACE inhibitors have detrimental effects on the unborn fetus and neonate. They are classified as pregnancy category C drugs for women in their first trimester and as pregnancy category D drugs for women in their second or third trimester. ACE inhibitors are to be used by pregnant women only if there are no safer alternatives. Fetal and neonatal morbidity and mortality have been reported to have occurred in at least 50 cases in which women received ACE inhibitors during their pregnancies.


Mechanism of Action and Drug Effects


The development of the ACE inhibitors was spurred by the discovery of an animal substance found to have beneficial effects in humans. This particular substance was the venom of a South American viper, which was found to inhibit kininase activity. Kininase is an enzyme that normally breaks down bradykinin, a potent vasodilator in the human body.


As their name implies, these drugs inhibit angiotensin-converting enzyme, which is responsible for converting AI (formed through the action of renin) to AII. AII is a potent vasoconstrictor and induces aldosterone secretion by the adrenal glands. Aldosterone stimulates sodium and water resorption, which can raise blood pressure. Together, these processes are referred to as the renin-angiotensin-aldosterone system. By inhibiting this process, blood pressure is lowered.


The primary effects of the ACE inhibitors are cardiovascular and renal. Their cardiovascular effects are due to their ability to reduce blood pressure by decreasing systemic vascular resistance (SVR). They do this by preventing the breakdown of the vasodilating substance bradykinin and also of substance P (another potent vasodilator), and preventing the formation of AII. These combined effects decrease afterload, or the resistance against which the left ventricle must pump to eject its volume of blood during contraction. The ACE inhibitors are beneficial in the treatment of heart failure because they prevent sodium and water resorption by inhibiting aldosterone secretion. This causes diuresis, which decreases blood volume and return to the heart. This in turn decreases preload, or the left ventricular end-diastolic volume, and the work required of the heart.


Indications


The therapeutic effects of the ACE inhibitors are related to their potent cardiovascular effects. They are excellent antihypertensives and adjunctive drugs for the treatment of heart failure. They may be used alone or in combination with other drugs such as diuretics in the treatment of hypertension or heart failure.


The beneficial hemodynamic effects of the ACE inhibitors have been studied extensively. Because of their ability to decrease SVR (a measure of afterload) and preload, ACE inhibitors can stop the progression of left ventricular hypertrophy, which is sometimes seen after a myocardial infarction (MI). This pathologic process is known as ventricular remodeling. The ability of ACE inhibitors to prevent this is termed a cardioprotective effect. ACE inhibitors have been shown to decrease morbidity and mortality in patients with heart failure. They are considered the drugs of choice for hypertensive patients with heart failure. ACE inhibitors also have been shown to have a protective effect on the kidneys, because they reduce glomerular filtration pressure. This is one reason that they are among the cardiovascular drugs of choice for diabetic patients. Numerous studies have shown that the ACE inhibitors reduce proteinuria, and they are considered by many to be standard therapy for diabetic patients to prevent the progression of diabetic nephropathy. The various therapeutic effects of the ACE inhibitors are listed in Table 22-3, which lists the biochemicals on which ACE inhibitors act and the resulting beneficial hemodynamic effects.


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May 9, 2017 | Posted by in NURSING | Comments Off on Antihypertensive Drugs

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