eMedicine Specialties > Nephrology > Hypertension and the Kidney

Hypertension: Treatment & Medication

Author: Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St. Boniface General Hospital
Coauthor(s): Claude Kortas, MD, Program Director, Associate Professor, Department of Medicine, University of Western Ontario, Canada
Contributor Information and Disclosures

Updated: Aug 6, 2008

Treatment

Medical Care

JNC VII recommendations to lower blood pressure and decrease cardiovascular disease risk include the following:

• Lose weight if overweight.
• Limit alcohol intake to no more than 1 oz (30 mL) of ethanol (ie, 24 oz [720 mL] of beer, 10 oz [300 mL] of wine, 2 oz [60 mL] of 100-proof whiskey) per day or 0.5 (15 mL) ethanol per day for women and people of lighter weight.
• Increase aerobic activity (30-45 min most days of the week).
• Reduce sodium intake to no more than 100 mmol/d (2.4 g sodium or 6 g sodium chloride).
• Maintain adequate intake of dietary potassium (approximately 90 mmol/d).
• Maintain adequate intake of dietary calcium and magnesium for general health.
• Stop smoking and reduce intake of dietary saturated fat and cholesterol for overall cardiovascular health.

Clinical trials

Multiple clinical trials suggest that most antihypertensive drugs provide the same degree of cardiovascular protection for the same level of blood pressure control. Well-designed prospective randomized trials, such as the Swedish Trial in Old Patients with Hypertension (STOP-2), the Nordic Diltiazem (NORDIL) trial, and the Intervention as a Goal in Hypertension Treatment (INSIGHT) trial, have shown a similar outcome with older drugs (eg, diuretics, beta-blockers) compared to the newer antihypertensive agents (eg, ACE inhibitors, calcium channel blockers).

No consensus exists regarding optimal drug therapy for treatment of hypertension; most clinicians recommend initiating therapy with a single agent and advancing to the low-dose combination therapy. Any of the first-line medications decrease blood pressure in 40-60% of patients with mild-to-moderate hypertension. In unresponsive patients, switching to a second drug (rather than combining it with the first drug) or switching to a third drug if the second drug is not effective may allow a 70-80% response rate to monotherapy. Therefore, attempt to identify a particular class of drug to which the patient responds rather than adding multiple drugs (as in combination therapy).

The JNC VII report recommends either a thiazide diuretic or a beta-blocker as the initial therapy of uncomplicated hypertension. A low dose of thiazide diuretic (12.5-25 mg hydrochlorothiazide) is a low-cost therapy with fewer complications, and it provides equivalent cardiovascular protection. Patients unresponsive to low-dose thiazide therapy should try an ACE inhibitor, beta-blocker, or calcium channel blocker, sequentially. Patients unresponsive to a diuretic may not respond to a calcium channel blocker, and an ACE inhibitor or a beta-blocker should be tried as a second-line agent in these patients. Calcium channel blocking agents and diuretics may be more effective in hypertensive black patients.

Initial therapy based on the JNC VII report recommendations is as follows:

• Prehypertension (systolic 120-139, diastolic 80-89): No antihypertensive drug is indicated.
• Stage 1 hypertension (systolic 140-159, diastolic 90-99): Thiazide-type diuretics are recommended for most. ACE inhibitor, angiotensin II receptor blocker (ARB), beta-blocker, calcium channel blocker, or combination may be considered.
• Stage 2 hypertension (systolic more than 160, diastolic more than 100): Two-drug combination (usually thiazide-type diuretic and ACE inhibitor or ARB or beta-blocker or calcium channel blocker) is recommended for most.
• For the compelling indications, other antihypertensive drugs (eg, diuretics, ACE inhibitor, ARB, beta-blocker, calcium channel blocker) may be considered as needed.

Randomized trials

Two randomized controlled trials, the Hypertension Detection and Follow-up Program (HDFP) and the Medical Research Council (MRC) trials, randomized patients with elevated levels of diastolic blood pressure to either diuretic-based stepped-care treatment or usual care. The usual care group received some form of therapy from their own physicians, whereas the stepped-care group received systematic care. In both studies, stepped-care treatment reduced diastolic blood pressure by 5 mm more than that reduced in the control group. Both trials showed a benefit from stepped-care therapy compared to the control group. In the HDFP trial, stepped-care led to relative risk reduction of 17% for total mortality; 76 hypertensive patients needed to be treated with stepped-care therapy for 5 years to prevent one death.

A meta-analysis published in the Journal of the American Medical Association (JAMA) in 1997 included several randomized controlled clinical trials. The total number of participants randomized to active therapy was 24,294, and the number for the control therapy was 23,926. Active treatment reduced diastolic blood pressure by at least 5 mm Hg. The meta-analysis showed a risk reduction of coronary heart disease of 8-14% and the reduction in stroke incidence of 35-40%. Subsequent meta-analysis reported that benefits of active treatment are similar in men and women.

Recommendations for management of hypertension

The JNC recommends certain situations for which a specific class of drug may be administered. An ACE inhibitor should be the initial treatment in situations in which hypertension is associated with congestive heart failure, diabetes mellitus with proteinuria, and postmyocardial infarction with systolic left ventricular dysfunction. In patients who develop persistent cough while on ACE inhibitor therapy, an angiotensin II receptor antagonist may be substituted, but these agents' efficacy in lowering cardiovascular mortality rates has not yet been proven. A beta-blocker should be prescribed following an acute myocardial infarction. A diuretic or a long-acting calcium channel blocker may be more effective in elderly patients with isolated systolic hypertension.

The 2004 Canadian Hypertension Society recommendations (similar to JNC VII guidelines) for the management of hypertension in specific patient groups are listed in Table 2 and Table 3, as follows:

Table 2. Synopsis of Considerations in the Use of Antihypertensive Drug Classes*

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*CMAJ 1999, 161:S1-S22

Table 3. Considerations in the Individualization of Antihypertensive Therapy*

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*Short-acting calcium channel blockers are not recommended in the treatment of hypertension

Several situations demand the addition of a second drug because 2 drugs may be used at lower doses to avoid adverse effects, which may occur with higher doses of an individual agent. Diuretics generally potentiate the effects of other antihypertensive drugs by minimizing volume expansion. Specifically, the use of the diuretic thiazide in conjunction with a beta-blocker or an ACE inhibitor has an additive effect, controlling blood pressure in up to 85% of patients.

Most drug combinations using agents that act by different mechanisms have an additive effect. The combination of a calcium channel blocker with either an ACE inhibitor or a dihydropyridine calcium channel blocker and a beta-blocker has additive effects. An ACE inhibitor may be combined with an angiotensin II receptor antagonist because the blocking of angiotensin I receptors may lead to increased plasma angiotensin II concentration, which may compete with a drug for the receptor. Some combinations may not be additive, including a beta-blocker and ACE inhibitor, a beta-blocker and an alpha1-blocker and an alpha2 stimulant, and, more controversially, a diuretic and a calcium channel blocker. Some combinations may have additive adverse effects; these include a beta-blocker combined with verapamil or diltiazem, which leads to cardiac depression, bradycardia, or heart block.

Clinical trials have shown that the effective control of blood pressure reduces the risk of cardiovascular events in high-risk patients. In the patients who achieved optimal blood pressure control compared with those with uncontrolled hypertension, significant reductions in the incidence of cardiac events, stroke, and all-cause mortality occurred (according to the Valsartan Antihypertensive Long-term Use Evaluation [VALUE] Trial). The lack of significant difference in cardiovascular mortality and morbidity among patients receiving diuretics, calcium channel blockers, or ACE inhibitors in the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) possibly occurred due to confounding because of differences in the blood pressure reductions achieved with the 3 treatments.

Recent studies have consistently shown that newer antihypertensive agents, such as ACE inhibitors and calcium channel blockers, reduce cardiovascular events to a similar, or possibly greater, extent as older therapies, such as diuretics and beta-blockers. ACE inhibitors specifically offer additional benefits beyond blood pressure reduction, which include reduction of cardiovascular events and renal protection. Similarly, ARBs have demonstrated beneficial effects in heart failure, stroke, and renal protection.

• Key messages of the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII) are as follows:
  • In those older than 50 years, systolic blood pressure (BP) of greater than 140 mm Hg is a more important cardiovascular disease risk factor than diastolic BP.
  • Beginning at 115/75 mm Hg, the cardiovascular disease risk doubles for each increment of 20/10 mm Hg.
  • Individuals who are normotensive at 55 years will have a 90% lifetime risk of developing hypertension.
  • Prehypertension (systolic 120-139, diastolic 80-89) requires health-promoting lifestyle modifications to prevent the progressive rise in blood pressure and cardiovascular disease.
  • In uncomplicated hypertension, a thiazide diuretic, either alone or combined with drugs from other classes, should be used for the drug treatment of most.
  • In specific high-risk conditions, there are compelling indications for the use of other antihypertensive drug classes (eg, ACE inhibitors, angiotensin-receptor blockers, beta-blockers, calcium channel blockers).
  • Two or more antihypertensive medications will be required to achieve goal BP (<140/90 mm Hg or <130/80 mm Hg) for patients with diabetes and chronic kidney disease.
  • For patients whose BP is more than 20 mm Hg above the systolic BP goal or more than 10 mm Hg above the diastolic BP goal, initiation of therapy using 2 agents, one of which usually will be a thiazide diuretic, should be considered.
  • Regardless of therapy or care, hypertension will be controlled only if patients are motivated to stay on their treatment plan.
• Resistant hypertension: Some patients may have persistent diastolic blood pressures above 100 mm Hg despite the use of 3 or more antihypertensive medications. These patients may be experiencing of the following factors as the cause of resistant hypertension:
  • Inadequate treatment was described as the most common cause of resistant hypertension in several published series. Patients may not be on an effective drug, or concomitant volume expansion may occur as a side effect of the drug.
  • Extracellular volume expansion: Volume expansion may contribute to the inability to lower systemic blood pressure. The volume expansion may occur because of renal insufficiency, sodium retention due to treatment with vasodilators, high-salt diet, or insufficient dosing of diuretic. This situation can be treated with more aggressive diuretic therapy until clinical signs of extracellular volume depletion (eg, orthostatic hypotension) develop.
  • Poor compliance: Noncompliance with medical therapy or dietary modifications (eg, salt restriction) may play a role in causing resistant hypertension. Address noncompliance with extensive patient education, simplification of the drug regimen, and use of drugs with the fewest adverse effects.
  • Secondary hypertension: Whenever confronted with resistant hypertension, try to exclude any secondary causes of hypertension. A reevaluation of the patient's history, physical examination, and laboratory results may provide clues to secondary hypertension (eg, renal artery stenosis, primary hyperaldosteronism).
  • White coat hypertension: Blood pressure rise secondary to anxiety may be observed in 20-30% of patients. This may be avoided by having patients rest prior to measurement, having a nurse check the blood pressure, or arranging to have the blood pressure monitored at home. Development of hypotensive symptoms on medications is an indication of white coat hypertension. White coat hypertension can also be evaluated by the use of a 24-hour ambulatory monitor.
• Pseudohypertension may be observed in elderly individuals who have thickened, calcified arteries. Much higher cuff pressure may be required to occlude a thickened brachial artery, and diastolic pressure may also be overestimated. Consider pseudohypertension in situations in which no organ damage occurs despite marked hypertension, when patients develop hypotensive systems on medications, and when calcification of the brachial artery is observed on radiologic examination. Direct measurement of intra-arterial pressure may be required in this setting.
• Vasoactive substances: Resistant hypertension may be encountered in patients who are ingesting vasoactive substances despite taking antihypertensive drugs regularly. Use of salt and alcohol are the common examples; others include use of cocaine, amphetamines, anabolic steroids, oral contraceptives, cyclosporine, antidepressants, and nonsteroidal anti-inflammatory drugs.
• Hypertension in special populations
  • Age
    • The systolic pressure continues to progressively rise throughout life, reaching the highest levels in later stages of life. Isolated systolic hypertension may be present in 10% of the population aged 70 years and in 24% of those aged 80 years. Furthermore, severe arteriosclerosis may lead to pseudohypertension. Isolated hypertension results in low cardiac output because of the decreased stroke volume and high peripheral resistance. This may reduce glomerular filtration further, which is why low activity of renal angiotensin aldosterone cascade is encountered in elderly individuals who are hypertensive.
    • Despite low PRA, blood pressure responds well to ACE inhibitor and angiotensin receptor inhibitor therapy. Low doses of diuretics may also be effective. Calcium antagonists are quite useful because of their strong antihypertensive effects. Often, combining 2 drugs at a lower dose may be preferable to using a single drug at a high dose that has the potential for adverse effects.
  • Sex: The prevalence of hypertension is similar between men and women, but women are protected from coronary heart disease prior to menopause. Premenopausal women have a higher resting heart rate, a higher cardiac index, and a lower peripheral resistance than men. These changes are not encountered in postmenopausal females. Therefore, in premenopausal situations, a medication such as beta-blocker may be effective. However, postmenopausal hypertension is treated similarly to that in men.
  • Race
    • Blacks have a higher prevalence of hypertension and a much higher frequency of end organ damage, such as occurs in end-stage renal disease, strokes, and heart failure. Black patients also develop more severe LVH than white patients. Renal function in hypertensive black patients continues to deteriorate over time despite aggressive management of the blood pressures.
    • Black patients respond less well to beta-blockers, ACE inhibitors, and angiotensin receptor blockers than white patients. At times, this relative lack of efficacy may be overcome by increasing the dosage of the medications. Blacks may respond well to treatment with calcium antagonists, diuretics, and postsynaptic alpha-blockers.
  • Obesity
    • Hypertensive patients who are obese have a higher cardiac output and a lower peripheral vascular resistance than hypertensive patients who are not obese. The increase in cardiac output manifests secondary to increased preload. The end-diastolic volume and pressure are elevated, leading to left ventricular dilatation. Left ventricular wall thickening also occurs secondary to increased afterload, which increases the risk of congestive heart failure. The concomitant diabetes often present in patients who are obese produces a devastating effect on kidneys and leads to a much higher incidence of renal failure.
    • No class of drugs seems to be of particular advantage in hypertensive patients who are obese, but thiazide diuretics may be helpful, unless the patient also has coexisting diabetes. In patients who are diabetic and who may have microalbuminuria, ACE inhibitors or calcium antagonists are recommended because they may slow declining renal function. Because of the high preload and afterload, drugs that have negative inotropic effects, such as beta-blockers, should be avoided.
• The management of secondary hypertension may result in cure by the surgical correction of the underlying problem, such as removal of a pheochromocytoma. Surgery may not be feasible in a substantial number of patients for whom medical therapy is instituted to control hypertension.
  • Renovascular hypertension
    • The goals of therapy are maintenance of normal blood pressure and prevention of end-stage renal disease. The therapeutic options include medical therapy, percutaneous transluminal renal angioplasty, and surgical revascularization. These options must be individualized because no randomized studies document the superiority of one option over the other. The indications for surgery or angioplasty include an inability to control blood pressure while on a medical regimen, the need to preserve renal function, and intolerable effects of medical therapy.
    • Aortal renal bypass using saphenus vein or hypogastric artery is a common revascularization technique. A synthetic graft has also been used. Percutaneous transluminal renal angioplasty (PTRA) can be effective treatment for both hypertension and preservation of renal function. PTRA may be the initial choice in younger patients with fibromuscular lesions amenable to balloon angioplasty. Renal artery stenting of osteal lesions has been associated with improved long-term patency. PTRA may also be used for arthrosclerotic renal artery stenosis; the outcome may be comparable to surgical revascularization. Medical therapy is required in the preoperative phase of interventional therapy. Medical therapy is also indicated for high-risk individuals and for older patients who have easily controlled hypertension.
    • ACE inhibitors are quite effective in patients with unilateral renal artery stenosis; however, avoid ACE inhibitors in patients with bilateral renal artery stenosis or stenosis of a solitary kidney. A diuretic can be combined with an ACE inhibitor. Because of their glomerular vasodilatory effect, calcium antagonists are effective in renal artery stenosis and do not compromise renal function.
  • Pheochromocytoma
    • Following suspicion of pheochromocytoma, the presence of a tumor should be confirmed biochemically by measuring urine and plasma concentrations of catecholamine or their metabolites. In most situations, a CT scan or an MRI may be used to localize the tumor in the abdomen. In the absence of abdominal imaging, nuclear scan with metaiodobenzylguanidine (MIBG) may further help with the localization.
    • Surgical resection is the treatment of choice because hypertension is cured by tumor resection. In the preoperative phase, combined alpha- and beta-adrenergic blockade is recommended for hypertension control. Alpha-adrenergic blockade is initiated with phenoxybenzamine or prazosin, and, following adequate alpha-adrenergic blockade, beta-adrenergic blockade is initiated. These patients are often volume contracted and require saline or sodium tablets. Catecholamines can be reduced further by metyrosine. For adrenal pheochromocytoma, laparoscopic adrenalectomy is becoming the procedure of choice in suitable patients. Follow-up 24-hour urinary excretion studies of catecholamines should be performed 2 weeks following surgery (and periodically thereafter) to detect recurrence, metastases, or development of second primary lesion.
  • Primary hyperaldosteronism
    • Hyperkalemia is an important clue to the presence of primary aldosteronism. However, in a subset of patients, the serum potassium concentration may be within the reference range. Measurement of PRA has been used as a screening test. A suppressed PRA value that fails to rise above 2 mg/mL/h after salt and water depletion is considered a positive test result. The best initial test is the determination of the aldosterone excretion rate during prolonged salt loading.
    • The appropriate therapy depends on the cause of excessive aldosterone production. A CT scan may help localize an adrenal mass, indicating adrenal adenoma. If the results of the CT scan are inconclusive, adrenal venous sampling for aldosterone and cortisol levels should be performed. Medical therapy is indicated in patients with adrenal hyperplasia, patients with adenoma who are poor surgical risks, and patients with bilateral adenomas. These patients are best treated with sustained salt and water depletion. Hydrochlorothiazide or furosemide in combination with either spironolactone or amiloride corrects hypokalemia and normalizes the blood pressure. Some patients may require the addition of a vasodilator or a beta-blocker for better control of hypertension.
    • Adrenal adenomas may be resected via a laparoscopic procedure. Surgical resection often leads to the control of blood pressure and the reversal of biochemical abnormalities. These patients may develop hypoaldosteronism during the postoperative follow-up period and require supplementation with fludrocortisone.

Surgical Care

Aortorenal bypass using saphenus vein graft or hypogastric artery is a common revascularization technique for renovascular hypertension. Surgical resection is the treatment of choice for pheochromocytoma because hypertension is cured by tumor resection. In patients with fibromuscular renal disease, angioplasty has a 60-80% success rate for cure or improvement of hypertension. Surgical correction of renal artery stenosis has resulted in cure of hypertension in approximately 61% of patients and amelioration in 27% of patients with fibromuscular lesions. With respect to renal artery stenosis secondary to atherosclerotic lesions, surgical correction has resulted in cure of hypertension in 38% of patients and amelioration in about 41% of patients. See Medical Care for more details.

Consultations

Consultations with a nutritionist and exercise specialist are often helpful in changing lifestyle and initiating weight loss. Consultations with an appropriate consultant are indicated for management of secondary hypertension attributable to a specific cause.

Diet

A number of studies have documented an association between sodium chloride intake and blood pressure. The effect of sodium chloride is particularly important in individuals who are middle-aged to elderly with a family history of hypertension. A moderate reduction in sodium chloride intake can lead to a small reduction in blood pressure. The American Heart Association recommends that the average daily consumption of sodium chloride not exceed 6 g, this may lower blood pressure by 2-8 mm Hg.

• The Dietary Approaches to Stop Hypertension (DASH) eating plan encompasses a diet rich in fruits, vegetables, and low-fat dairy products and may lower blood pressure by 8-14 mm Hg.²
• Dietary potassium, calcium, and magnesium consumption have an inverse association with blood pressures. Lower intake of these elements potentiates the affect of sodium on blood pressure. Oral potassium supplementation may lower both systolic and diastolic pressure. Calcium and magnesium supplementation have elicited small reductions in blood pressures.
• In population studies, low levels of alcohol consumption have shown a favorable effect on blood pressure, with reductions of 2-4 mm Hg. However, the consumption of 3 or more drinks per day is associated with elevation of blood pressure. Alcohol intake should be restricted to less than 1 oz of ethanol in men and 0.5 oz in women.
• Weight reduction may lower blood pressure by 5-20 mm Hg per 10 kg of weight loss in a patient who weighs more than 10% of ideal body weight.

Activity

Up to 60% of all individuals with hypertension are more than 20% overweight. The centripetal fat distribution is associated with insulin resistance and hypertension. Even modest weight loss (5%) can lead to reduction in blood pressure and improved insulin sensitivity. Regular aerobic physical activity can facilitate weight loss, decrease blood pressure, and reduce the overall risk of cardiovascular disease. Blood pressure may be lowered by 4-9 mm Hg with moderately intense physical activity. These activities include brisk walking for 30 minutes a day, 5 days per week. More intense workouts for 20-30 minutes, 3-4 times a week may also lower blood pressure and have additional health benefits.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Diuretics

Cause diuresis, which decreases plasma volume and edema, thereby decreasing cardiac output and blood pressure.

Hydrochlorothiazide (Esidrix, HydroDIURIL, Microzide)

Inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium, water, potassium, and hydrogen ions.

Spironolactone (Aldactone)

Used for management of hypertension. May block effects of aldosterone on arteriolar smooth muscles.

Amiloride (Midamor)

l-carbonyl-guanidine unrelated chemically to other known antikaliuretic or diuretic agents. Potassium-conserving (antikaliuretic) drug that, compared with thiazide diuretics, possesses weak natriuretic, diuretic, and antihypertensive activity.

Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Dose must be individualized to patient. Depending on response, administer at increments of 20-40 mg no sooner than 6-8 h after previous dose until desired diuresis occurs. When treating infants, titrate with 1-mg/kg per dose increments until satisfactory effect achieved.

Alpha1-adrenergic blockers

Selectively block postsynaptic alpha1-adrenergic receptors. Dilate arterioles and veins, thus lowering blood pressure.

Prazosin (Minipress), Terazosin (Hytrin)

Prazosin treats prostatic hypertrophy. Improves urine flow rates by relaxing smooth muscle, which is caused by blocking alpha1-adrenoceptors in bladder neck and prostate. When increasing dose, administer first dose of each increment at bedtime to reduce syncopal episodes. Although doses >20 mg/d usually do not increase efficacy, some patients may benefit from as much as 40 mg/d.
Terazosin decreases arterial tone by allowing peripheral postsynaptic blockade. Has minimal alpha2 effect.

Beta-adrenergic blocking agents

Used to treat hypertension as initial agents or in combination with other drugs (eg, thiazides).

Atenolol (Tenormin), Metoprolol (Lopressor, Toprol XL), Propranolol (Inderal), Nebivolol (Bystolic)

Atenolol and metoprolol selectively block beta1-receptors with little or no effect on beta2 types.
Propranolol is a class II antiarrhythmic, nonselective, beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions.
Nebivolol actions depend on metabolic factors and dose. In extensive metabolizers (majority of the population) and doses <10 mg, preferentially elicits beta1 selective inhibition, whereas in poor metabolizers and at higher doses, inhibits both beta1- and beta2-receptors.

Alpha/beta-adrenergic blocking agents

Block alpha-, beta1-, and beta2-adrenergic receptor sites, thus decreasing blood pressure.

Labetalol (Normodyne, Trandate), Carvedilol (Coreg)

Nonselective beta- and alpha-adrenergic blockers. Do not appear to have intrinsic sympathomimetic activity. May reduce cardiac output and decrease peripheral vascular resistance. Use in aortic dissection not advisable when titratable drugs, such as esmolol and nitroprusside, available.

Peripheral vasodilators

Relax blood vessels to improve blood flow, thus decreasing blood pressure.

Hydralazine (Apresoline), Minoxidil (Rogaine Loniten)

Hydralazine decreases systemic resistance through direct vasodilation of arterioles.
Minoxidil relaxes arteriolar smooth muscle, causing vasodilation, which, in turn, may reduce blood pressure.

Calcium channel blockers

May be a more effective class of medication for black patients.

Diltiazem (Cardizem, Dilacor), Verapamil (Calan, Covera-HS), Nifedipine (Adalat)

During depolarization, inhibits calcium ion from entering slow channels or voltage-sensitive areas of vascular smooth muscle and myocardium.

Angiotensin-converting enzyme (ACE) inhibitors

Competitive inhibitors of ACE. Reduces angiotensin II levels, thus decreasing aldosterone secretion.

Captopril (Capoten), Enalapril (Vasotec), Lisinopril (Zestril), Ramipril (Altace)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

Angiotensin II receptor antagonists

For patients unable to tolerate ACE inhibitors.

Losartan (Cozaar), Valsartan (Diovan)

Nonpeptide angiotensin II receptor antagonists that block vasoconstrictor and aldosterone-secreting effects of angiotensin II. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors, do not affect response to bradykinin, and are less likely to be associated with cough and angioedema.

Eprosartan (Teveten), Olmesartan (Benicar)

Angiotensin receptor antagonist that binds to AT1 angiotensin II receptor, blocking vasoconstrictor and aldosterone-secreting effects of angiotensin II. May induce a more complete inhibition of renin-angiotensin system than ACE inhibitors and do not affect response to bradykinin and, thus, is less likely to be associated with cough and angioedema. For patients unable to tolerate ACE inhibitors.

Aldosterone antagonists

Compete with aldosterone receptor sites, reducing blood pressure and sodium reabsorption.

Eplerenone (INSPRA)

Selectively blocks aldosterone at the mineralocorticoid receptors in epithelial (eg, kidney) and nonepithelial (eg, heart, blood vessels, brain) tissues, thus decreasing blood pressure and sodium reabsorption.

Alpha-adrenergic agonists

Stimulate presynaptic alpha2-adrenergic receptors in the brain stem, which reduces sympathetic nervous activity.

Methyldopa (Aldomet)

Stimulates central alpha-adrenergic receptors by a false transmitter, resulting in decreased sympathetic outflow. This results in inhibition of vasoconstriction.

Clonidine (Catapres)

Stimulates alpha2-adrenoreceptors in brain stem, activating an inhibitory neuron, which, in turn, results in reduced sympathetic outflow. These effects result in a decrease in vasomotor tone and heart rate.

Renin inhibitor

Newest class of antihypertensive drugs. Acts by disrupting the renin-angiotensin-aldosterone system feedback loop.

Aliskiren (Tekturna)

Direct renin inhibitor. Decreases plasma renin activity and inhibits conversion of angiotensinogen to angiotensin I (as a result, also decreasing angiotensin II) and, thereby, disrupts the renin-angiotensin-aldosterone system (RAAS) feedback loop. Indicated for hypertension as monotherapy or in combination with other antihypertensive drugs.

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