Antihypertensive
Antihypertensives are a class of drugs that are used to treat hypertension. Antihypertensive therapy seeks to prevent the complications of high blood pressure, such as stroke, heart failure, kidney failure and myocardial infarction. Evidence suggests that a reduction of blood pressure by 5 mmHg can decrease the risk of stroke by 34% and of ischaemic heart disease by 21%. It can reduce the likelihood of dementia, heart failure, and mortality from cardiovascular disease. There are many classes of antihypertensives, which lower blood pressure by different means. Among the most important and most widely used medications are thiazide diuretics, calcium channel blockers, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers or antagonists, and beta blockers.
Which type of medication to use initially for hypertension has been the subject of several large studies and resulting national guidelines. The fundamental goal of treatment should be the prevention of the important endpoints of hypertension, such as heart attack, stroke and heart failure. Patient age, associated clinical conditions and end-organ damage also play a part in determining dosage and type of medication administered. The several classes of antihypertensives differ in side effect profiles, ability to prevent endpoints, and cost. The choice of more expensive agents, where cheaper ones would be equally effective, may have negative impacts on national healthcare budgets. As of 2018, the best available evidence favors low-dose thiazide diuretics as the first-line treatment of choice for high blood pressure when drugs are necessary. Although clinical evidence shows calcium channel blockers and thiazide-type diuretics are preferred first-line treatments for most people, an ACEi is recommended by NICE in the UK for those under 55 years old.
Diuretics
s help the kidneys eliminate excess salt and water from the body's tissues and blood.- Loop diuretics:
- * bumetanide
- * ethacrynic acid
- * furosemide
- * torsemide
- Thiazide diuretics:
- * epitizide
- * hydrochlorothiazide and chlorothiazide
- * bendroflumethiazide
- * methyclothiazide
- * polythiazide
- Thiazide-like diuretics:
- * indapamide
- * chlorthalidone
- * metolazone
- * xipamide
- * clopamide
- Potassium-sparing diuretics:
- * amiloride
- * triamterene
- * spironolactone
- * eplerenone
Medications that are classified as potassium-sparing diuretics which block the epithelial sodium channel, such as amiloride and triamterene, are seldom prescribed as monotherapy. ENaC blocker medications need stronger public evidence for their blood pressure reducing effect.
Calcium channel blockers
s block the entry of calcium into muscle cells in artery walls, resulting in the relaxation of muscle cells and vasodilation.- dihydropyridines:
- * amlodipine
- * barnidipine
- * cilnidipine
- * clevidipine
- * felodipine
- * isradipine
- * lercanidipine
- * levamlodipine
- * nicardipine
- * nifedipine
- * nimodipine
- * nisoldipine
- * nitrendipine
- non-dihydropyridines:
- * diltiazem
- * verapamil
The ratio of CCBs' anti-proteinuria effect, non-dihydropyridine to dihydropyridine was 30 to −2. The anti-proteinuria effect of non-dihydropyridine is due to better selectivity during glomerular filtration and/or a lower perfusion rate through the renal system.
Notable side effects of CCBs include edema, flushing in the face, headache, drowsiness, and dizziness.
ACEis
ACEis inhibit the activity of angiotensin-converting enzyme, an enzyme responsible for the conversion of angiotensin I into angiotensin II, a potent vasoconstrictor.- captopril
- enalapril
- fosinopril
- lisinopril
- moexipril
- perindopril
- quinapril
- ramipril
- trandolapril
- benazepril
However, ACEis should not be a first-line treatment for black hypertensives without chronic kidney disease. Results from the ALLHAT trial showed that thiazide-type diuretics and calcium channel blockers were both more effective as monotherapy in improving cardiovascular outcomes compared to ACEis for this subgroup. Furthermore, ACEis were less effective in reducing blood pressure and had a 51% higher risk of stroke in black hypertensives when used as initial therapy compared to a calcium channel blocker. There are fixed-dose combination drugs, such as ACE inhibitor and thiazide combinations.
Notable side effects of ACEis include dry cough, high blood levels of potassium, fatigue, dizziness, headaches, loss of taste and a risk for angioedema.
ARBs
ARBs work by antagonizing the activation of angiotensin receptors.In 2004, an article in the BMJ examined the evidence for and against the suggestion that ARBs may increase the risk of myocardial infarction. The matter was debated in 2006 in the medical journal of the American Heart Association. There is no consensus on whether ARBs have a tendency to increase MI, but there is also no substantive evidence to indicate that ARBs are able to reduce MI.
In the VALUE trial, the ARB valsartan produced a statistically significant 19% relative increase in the prespecified secondary end point of myocardial infarction compared with amlodipine.
The CHARM-alternative trial showed a significant +52% increase in myocardial infarction with candesartan despite a reduction in blood pressure.
As a consequence of AT1 blockade, ARBs increase angiotensin II levels several-fold above baseline by uncoupling a negative-feedback loop. Increased levels of circulating angiotensin II result in unopposed stimulation of the AT2 receptors, which are, in addition upregulated. Recent data suggest that AT2 receptor stimulation may be less beneficial than previously proposed and may even be harmful under certain circumstances through mediation of growth promotion, fibrosis, and hypertrophy, as well as proatherogenic and proinflammatory effects.
An ARB happens to be the favorable alternative to an ACEi if a hypertensive patient with the heart-failure type of reduced ejection fraction treated with an ACEi was intolerant of cough, angioedema other than hyperkalemia or chronic kidney disease.
Adrenergic receptor antagonists
Beta-blockers can block beta-1 adrenergic receptors and/or beta-2 adrenergic receptors. Those that block beta-1-adrenergic receptors prevent the binding of endogenous catecholamines, which ultimately reduces blood pressure through decreasing renin and cardiac output release. Those that block beta-2-adrenergic receptors reduce blood pressure through increased relaxation of smooth muscle.Alpha-blockers can block alpha-1 adrenergic receptors and/or alpha-2 adrenergic receptors. Those that block alpha-1-adrenergic receptors on vascular smooth muscle cells prevent vasoconstriction. Blockade of alpha-2-adrenergic receptors prevents the negative feedback mechanism of norepinephrine. Non-selective alpha-blockers generate a balance whereby alpha-2-blockers release NE to reduce the vasodilation effects induced by alpha-1-blockers.
- Beta blockers
- * acebutolol
- * atenolol
- * bisoprolol
- * betaxolol
- * carteolol
- * carvedilol
- * labetalol
- * metoprolol
- * nadolol
- * nebivolol
- * oxprenolol
- * penbutolol
- * pindolol
- * propranolol
- * timolol
- Alpha blockers:
- * doxazosin
- * chlorpromazine
- * phentolamine
- * indoramin
- * phenoxybenzamine
- * prazosin
- * terazosin
- * tolazoline
- * urapidil
- Mixed Alpha + Beta blockers:
- * bucindolol
- * carvedilol
- * labetalol
- * clonidine
Despite lowering blood pressure, alpha blockers have significantly poorer endpoint outcomes than other antihypertensives, and are no longer recommended as a first-line choice in the treatment of hypertension.
However, they may be useful for some men with symptoms of prostate disease.