Every antihypertensive class side by side: how it lowers pressure, what it does to heart rate and potassium, when to reach for it, its signature adverse effect and when to avoid it.
| Class and examples | Where and how it lowers blood pressure | Heart rate, potassium and other labs | Best used for | Signature adverse effect | Do not use / avoid | Source |
|---|---|---|---|---|---|---|
| ACE (angiotensin-converting enzyme) inhibitors -pril: captopril, lisinopril, enalapril, ramipril | Blocks ACE: less angiotensin II, so less vasoconstriction, less aldosterone, less sodium reabsorption, less norepinephrine release. Slows bradykinin breakdown. | Raises potassium (hyperkalemia, worst with kidney disease, potassium-sparing diuretics, potassium supplements, salt substitutes). Can drop the glomerular filtration rate. | Hypertension (preferred in diabetics), heart failure and left ventricular dysfunction, after a myocardial infarction, diabetic nephropathy. | Dry cough (5–15%); angioedema (0.1–0.5%). | Pregnancy (second and third trimesters). Caution in kidney disease; nonsteroidal anti-inflammatory drugs blunt the effect. | L6 slide 20 slide 11 |
| Angiotensin receptor blockers -sartan: losartan, valsartan, candesartan | Blocks the angiotensin II type 1 (AT1) receptor: vasodilation, less aldosterone, less sodium reabsorption, less norepinephrine release. Does not inhibit bradykinin breakdown. | Raises potassium (kidney disease or potassium-sparing diuretics). Can impair kidney function. | Hypertension; left ventricular dysfunction when an ACE (angiotensin-converting enzyme) inhibitor is not tolerated; diabetic nephropathy. | No cough; lower incidence of angioedema than ACE inhibitors. | Pregnancy (not given in the second and third trimesters). Start low in heart failure. | L6 slide 29 slide 25 slide 26 |
| Dihydropyridine calcium channel blockers -dipine: amlodipine, nifedipine, nicardipine, felodipine, isradipine, nisoldipine, nimodipine | Block L-type channels in arterial smooth muscle: vasodilation, decrease afterload, no effect on preload. Little effect on the heart itself. | Reflex (rebound) tachycardia; no effect on atrioventricular conduction (suppression of contractility 0/+). | Hypertension; angina (amlodipine, nifedipine, nicardipine); nimodipine for subarachnoid hemorrhage. | Peripheral edema, dyspnea, wheezing, rebound tachycardia; gingival hyperplasia. | Severe aortic stenosis; unstable angina or recent myocardial infarction (immediate-release form). Avoid short-acting formulations. | L6 slide 51 slide 38 slide 40 slide 42 |
| Non-dihydropyridine calcium channel blockers diltiazem, verapamil | Block L-type channels in vessels and in the heart: slow inward current and rate of recovery both fall, slowing atrioventricular conduction and contractility. | Slow the heart rate (bradycardia); inhibit cytochrome P450 3A4 and P-glycoprotein, raising statins, digoxin, tacrolimus, cyclosporine and carbamazepine; can raise liver-function tests. | Hypertension, angina, supraventricular tachycardia, atrial fibrillation or flutter. | Bradycardia, atrioventricular block, worsening heart failure; constipation. | Advanced heart block; hypotension. Relative: heart failure, liver disease, gastroesophageal reflux disease. | L6 slide 46 slide 40 |
| Beta blockers -olol: metoprolol, atenolol, propranolol, carvedilol | Block cardiac beta-1 (lower cardiac output, with an acute reflex rise in peripheral resistance) and the beta-1 receptors that release renin (less angiotensin II); central effects lower sympathetic activity. | Lower heart rate; raise triglycerides; in diabetes they mask and prolong hypoglycemia and can raise glucose. | Not first-line for hypertension. Compelling indications: heart failure (carvedilol, metoprolol succinate, bisoprolol), after a myocardial infarction, angina, arrhythmias, glaucoma, migraine, hyperthyroidism, tremor. | Sudden withdrawal syndrome; bronchospasm; bradycardia and heart block; fatigue. | Bronchospasm (asthma, chronic obstructive pulmonary disease). Never stop suddenly. | L6 slide 71 slide 56 slide 57 |
| Alpha-1 blockers -zosin: prazosin, terazosin, doxazosin; tamsulosin is alpha-1A | Block vascular alpha-1 receptors: dilate precapillary arterioles and lower total peripheral resistance. | Reflex tachycardia (mild), raised renin with sodium and water retention; prazosin mildly lowers low-density lipoprotein cholesterol and triglycerides and raises high-density lipoprotein cholesterol. | Add-on for hypertension (with beta blockers and diuretics); benign prostatic hyperplasia (terazosin, doxazosin, tamsulosin). | Orthostatic hypotension and postural dizziness; impotence. | Caution in cardiac and renal failure; nonsteroidal anti-inflammatory drugs attenuate the response; beta blockers add to postural hypotension. | L6 slide 79 slide 77 |
| Central sympatholytics clonidine, guanfacine | Stimulate central alpha-2 receptors (and imidazoline receptors): less sympathetic outflow, so lower resistance, heart rate and cardiac output. | Lower heart rate; clonidine raises blood glucose and causes sodium retention; no negative effect on lipids. | Can be used as monotherapy: efficacy is independent of age, race and gender and they work well in the elderly (advantages, not first-line); clonidine also blunts opiate withdrawal. | Abrupt withdrawal hypertension; drowsiness, dry mouth. | Do not stop suddenly. Narrow therapeutic range; with a beta blocker the rebound is greater. | L6 slide 91 slide 86 slide 89 |
| Direct vasodilators hydralazine, minoxidil | Dilate arterioles directly (hydralazine: mechanism not fully clear, with raised cyclic guanosine monophosphate through nitric oxide as one proposal; minoxidil: opens potassium channels, causing hyperpolarization and relaxation). | Reflex tachycardia, higher cardiac output, fluid retention, raised renin, tachyphylaxis. | Chronic hypertension with a diuretic and a beta blocker (hydralazine); minoxidil as triple therapy for severe or refractory hypertension. | Hydralazine lupus syndrome, black stools; minoxidil hypertrichosis, myocardial ischemia, arrhythmias. | Hydralazine: coronary artery disease and ischemia. Use caution in the elderly. | L6 slide 99 slide 100 slide 103 |
| Nitroprusside intravenous vasodilator | Releases nitric oxide (one nitric oxide and five cyanide groups on iron): cyclic guanosine monophosphate rises, intracellular calcium falls. Dilates veins and arterioles. | Reflex tachycardia can occur, as with other direct vasodilators; the toxic metabolites cyanide and thiocyanate build up with long infusions or kidney failure. | Hypertensive crisis, by intravenous infusion. | Cyanide toxicity (trembling, vomiting, convulsions); thiocyanate toxicity. | Limit long infusions and use in kidney failure; give sodium thiosulfate to limit cyanide toxicity. | L6 slide 107 |