Antihypertensive Drugs Pharmacology for NEET PG 2026: Classes, DOC, ADRs

Hypertension is the most common chronic condition in adult Indian medicine practice, and antihypertensive pharmacology is correspondingly the densest NEET PG block of drug-class questions. Examiners reach for it because each class has clean indications, contraindications, and signature ADRs that map onto vignettes — and because the pregnancy and CKD subsets reward students who memorise drug-of-choice tables well.

This NEETPGAI deep dive walks through every major class, mechanism, side-effect profile, drug-of-choice scenarios, and the IV agents used in hypertensive emergency. Pair this guide with the heart failure deep dive and the dyslipidemia and statins guide for a complete preventive-cardiology pharmacology map.

ACE inhibitors

Mechanism — block angiotensin-converting enzyme (kininase II), reducing angiotensin II and aldosterone, increasing bradykinin. Result: arterial and venous vasodilation, reduced afterload, natriuresis, and antifibrotic remodelling.

Examples — captopril, enalapril, ramipril, lisinopril, perindopril, trandolapril.

Indications — hypertension, HFrEF, post-MI, diabetic nephropathy, CKD with proteinuria, secondary stroke prevention.

ADRs

• Dry cough (5 to 20 percent) — bradykinin-mediated.
• Angioedema — rare but life-threatening; switch to ARB only after caution as ARB can rarely cause it too.
• Hyperkalaemia — especially with K-sparing diuretics or NSAIDs.
• Acute kidney injury in bilateral renal artery stenosis.
• Foetal toxicity — renal dysgenesis, oligohydramnios, hypocalvaria. Absolutely contraindicated in pregnancy.
• First-dose hypotension.
• Loss of taste (dysgeusia, especially captopril — sulfhydryl group).

Drug interactions — NSAIDs (reduced efficacy plus AKI), potassium-sparing diuretics (hyperkalaemia), lithium (toxicity).

Angiotensin receptor blockers

Mechanism — competitive antagonism at AT1 receptor without affecting bradykinin metabolism, hence less cough.

Examples — losartan, valsartan, candesartan, irbesartan, telmisartan, olmesartan.

Indications — same as ACEi; preferred when ACEi-induced cough is troublesome.

ADRs

• Hyperkalaemia.
• Acute kidney injury in bilateral renal artery stenosis.
• Foetal toxicity — same contraindication in pregnancy.
• Angioedema is rare.
• Olmesartan-induced sprue-like enteropathy.

The ONTARGET trial showed combining ACEi plus ARB increases adverse events without reducing mortality — never combine.

Calcium channel blockers

CCBs split into dihydropyridines (vascular-selective) and non-dihydropyridines (cardiac-selective).

Dihydropyridines

Examples — amlodipine, nifedipine, felodipine, nicardipine, clevidipine, isradipine.

Mechanism — block L-type calcium channels in vascular smooth muscle, causing arterial vasodilation.

Indications — hypertension (especially elderly and isolated systolic), angina, Raynaud, subarachnoid haemorrhage vasospasm prevention (nimodipine — penetrates CNS).

ADRs — peripheral oedema (capillary leak from arteriolar dilation, NOT volume overload — diuretics don't help; switch class or add ACEi/ARB), reflex tachycardia (short-acting nifedipine), gingival hyperplasia, flushing, headache.

Non-dihydropyridines

Examples — verapamil (most cardiac-selective), diltiazem.

Mechanism — slow AV node conduction, reduce heart rate and contractility in addition to mild arterial vasodilation.

Indications — hypertension, supraventricular tachycardia, atrial fibrillation rate control, vasospastic angina.

ADRs

• Bradycardia and AV block.
• Constipation (especially verapamil — calcium-mediated GI smooth muscle relaxation).
• Negative inotropy — avoid in HFrEF.
• Gingival hyperplasia.
• Drug interactions — verapamil and diltiazem are CYP3A4 inhibitors, raising statin and digoxin levels.

Never combine non-DHP CCB with a beta-blocker due to additive AV block and bradycardia.

Beta-blockers

Beta-blockers were demoted from first-line for uncomplicated hypertension by JNC 8 and NICE 2019 because they are less effective at stroke prevention than ACEi/ARB or CCB. They remain pivotal for compelling indications.

Cardioselective (beta-1 selective) — bisoprolol, esmolol, atenolol, metoprolol, nebivolol (also NO-mediated vasodilation). Mnemonic BEAM-N. Preferred in asthma, COPD, peripheral vascular disease, diabetes (less metabolic disturbance).

Non-selective — propranolol (most lipophilic; CNS effects, useful in essential tremor, performance anxiety, migraine prophylaxis), nadolol, timolol (glaucoma drops can cause systemic ADRs in elderly), pindolol, sotalol (also class III antiarrhythmic).

Mixed alpha-beta blockers — labetalol (1:3 alpha:beta blockade orally, 1:7 IV; pregnancy DOC, hypertensive emergency), carvedilol (added antioxidant effect; HF and HTN).

Beta-blockers with intrinsic sympathomimetic activity (ISA) — pindolol, acebutolol. Less bradycardia and dyslipidemia. Avoid in post-MI and HF.

Indications

• Compelling: HFrEF (carvedilol, metoprolol succinate, bisoprolol — only three with mortality data), post-MI, atrial fibrillation rate control, performance anxiety, essential tremor, hyperthyroidism (propranolol), portal hypertension prophylaxis, glaucoma (timolol).
• Hypertension (only with compelling indication or after first-line classes failed).

ADRs

• Bradycardia and AV block.
• Bronchospasm — non-selective worse; cardioselective acceptable in mild-moderate asthma.
• Mask hypoglycaemia symptoms in diabetics.
• Erectile dysfunction.
• Cold extremities, fatigue.
• Worsen Raynaud and PVD.
• Dyslipidemia (raised triglycerides, lower HDL — least with carvedilol and nebivolol).
• Abrupt withdrawal — rebound angina and tachycardia from upregulated receptors. Always taper.

Diuretics

Thiazides

Examples — hydrochlorothiazide, chlorthalidone (longer half-life, more potent for ASCVD outcome), indapamide, metolazone.

Mechanism — block Na-Cl symporter in distal convoluted tubule, mild natriuresis, plus a vasodilator effect that emerges over weeks.

Indications — hypertension (first-line in JNC 8 in non-Black patients without diabetes/CKD), osteoporosis (raises serum calcium), nephrogenic diabetes insipidus (paradoxical reduction of urine volume), recurrent calcium oxalate kidney stones.

ADRs (mnemonic hyperGLUC) — hyperGlycaemia, hyperLipidemia, hyperUricaemia, hyperCalcaemia, plus hypokalaemia, hyponatraemia, metabolic alkalosis, sulfa allergy, photosensitivity. Avoid eGFR under 30 mL/min (use loop instead).

Loop diuretics

Examples — furosemide, torsemide, bumetanide, ethacrynic acid (only loop without sulfa group).

Mechanism — block Na-K-2Cl symporter in thick ascending limb.

Indications — pulmonary oedema, HFrEF symptom control, oliguric AKI, hypercalcaemia (with saline).

ADRs (mnemonic OH DANG) — Ototoxicity (especially fast IV ethacrynic acid), Hypokalaemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout. Plus hypocalcaemia and metabolic alkalosis.

Potassium-sparing diuretics

Examples — spironolactone, eplerenone (selective MRA, less gynecomastia), amiloride, triamterene.

Mechanism — spironolactone and eplerenone antagonise aldosterone receptor in the cortical collecting duct; amiloride and triamterene block ENaC sodium channels.

Indications — primary hyperaldosteronism (Conn's syndrome), secondary hyperaldosteronism (cirrhosis ascites — spironolactone first-line), HFrEF (RALES, EPHESUS), resistant hypertension (PATHWAY-2 — spironolactone is fourth-line drug of choice).

ADRs — hyperkalaemia, gynecomastia (spironolactone), menstrual irregularities, anti-androgen effects (impotence, hirsutism), metabolic acidosis. Eplerenone is preferred when gynecomastia is troublesome.

Alpha-1 blockers

Examples — prazosin, terazosin, doxazosin, tamsulosin (uroselective — alpha-1A).

Indications — benign prostatic hyperplasia (preferred), hypertension (rarely first-line; ALLHAT showed worse heart-failure outcomes than chlorthalidone), PTSD nightmares (prazosin), pheochromocytoma pre-operative blockade.

ADRs — first-dose orthostatic hypotension (start at bedtime), dizziness, reflex tachycardia, intra-operative floppy iris syndrome (tamsulosin — surgeon must know before cataract surgery).

Centrally acting agents

Methyldopa — converted to alpha-methylnorepinephrine, an alpha-2 agonist that reduces sympathetic outflow. Pregnancy-safe. ADRs: positive direct Coombs test (haemolytic anaemia), hepatotoxicity, drug-induced lupus, sedation, dry mouth.

Clonidine — central alpha-2 agonist. Used in resistant hypertension, opioid and alcohol withdrawal, ADHD, and clonidine-suppression test for pheochromocytoma. Abrupt withdrawal causes rebound hypertension — taper carefully.

Direct vasodilators

Hydralazine — arteriolar vasodilator. Indications: severe hypertension in pregnancy, hypertensive emergency, HFrEF (with isosorbide dinitrate, especially in self-identified Black patients — A-HeFT trial). ADRs: drug-induced lupus (slow acetylators), reflex tachycardia, fluid retention.

Minoxidil — opens K-ATP channels, severe vasodilator. Reserved for refractory hypertension with hair loss as a fortunate side effect (topical formulation marketed for alopecia). ADRs: hypertrichosis, pericardial effusion, severe fluid retention requiring loop diuretic plus beta-blocker.

Sodium nitroprusside — direct NO donor with rapid onset and offset; IV only. Indications: hypertensive emergency, especially aortic dissection (with esmolol), acute decompensated HF. ADRs: cyanide and thiocyanate toxicity (manifest as metabolic acidosis, altered mentation, seizures); avoid more than 48 to 72 hours and in renal failure. Use cobalamin or hydroxocobalamin antidote.

Nitroglycerin — predominantly venous vasodilator at low doses (preload reduction), arterial at high doses. Acute coronary syndrome, pulmonary oedema, hypertensive emergency with HF or ACS.

Drug of choice tables

Compelling indications

Hypertensive emergency drugs

NEET PG MCQ traps

1. Pregnancy contraindication — ACEi, ARB, and direct renin inhibitors (aliskiren) all cause foetopathy. Never give in pregnancy.
2. Spironolactone gynecomastia — switch to eplerenone.
3. Verapamil plus beta-blocker — additive AV block; never combine routinely.
4. Cocaine-associated chest pain — beta-blocker monotherapy causes unopposed alpha vasoconstriction; use phentolamine or nicardipine instead.
5. Bilateral renal artery stenosis — ACEi/ARB cause AKI; pick CCB or alpha-blocker.
6. DHP-induced oedema — does NOT respond to diuretics; switch class or add ACEi/ARB.
7. Methyldopa Coombs test — positive in 20 percent, haemolysis in 1 percent.
8. Hydralazine slow acetylators — drug-induced lupus risk.
9. Clonidine rebound — severe hypertension if abruptly stopped; taper over 1 to 2 weeks.
10. Nitroprusside cyanide toxicity — high-anion-gap metabolic acidosis with elevated lactate; treat with hydroxocobalamin.
11. Tamsulosin and cataract surgery — intra-operative floppy iris; warn ophthalmologist.
12. Atenolol versus metoprolol succinate — atenolol is renally cleared and has no mortality benefit in HFrEF; metoprolol succinate (extended release) is the only metoprolol formulation with HF mortality data.

Recent updates and Indian context

• JNC 8 / NICE 2019 — first-line classes for uncomplicated hypertension are thiazide, ACEi/ARB, or DHP CCB; beta-blockers are no longer first-line.
• PATHWAY-2 (2015) — spironolactone is the most effective fourth-line drug in resistant hypertension.
• SPRINT (2015) — intensive BP target under 120 mmHg systolic reduces cardiovascular events but increases AKI and syncope.
• HOPE-3 — moderate-intensity statin plus candesartan plus hydrochlorothiazide gave broad CV benefit in intermediate-risk patients.
• Indian Society of Hypertension (ISH) 2020 — endorses combination first-line therapy (ACEi/ARB plus CCB or thiazide) for stage 2 hypertension; reflects the high rate of poor control on monotherapy in India.
• NMC and FMGE alignment — Indian undergraduate exams emphasise pregnancy DOC, CKD-proteinuria DOC, hypertensive emergency drugs, and the metabolic side-effect comparison among diuretics.
• Salt reduction — Indian average sodium intake exceeds 8 g/day; the FSSAI 2024 push to label and reduce salt is a public-health pharmacology adjunct that occasionally appears in PSM-style stems.

Frequently asked questions

What is the drug of choice for hypertension in pregnancy?

Labetalol is first-line oral therapy in pregnancy because it crosses the placenta minimally and does not cause foetal bradycardia at usual doses. Methyldopa, nifedipine sustained-release, and hydralazine are alternatives. ACE inhibitors, ARBs, and direct renin inhibitors are absolutely contraindicated in pregnancy due to foetal renal agenesis, oligohydramnios, and hypocalvaria.

Which beta-blockers are cardioselective?

Cardioselective beta-blockers selectively block beta-1 receptors at standard doses. The mnemonic is BEAM-N: Bisoprolol, Esmolol, Atenolol, Metoprolol, Nebivolol. Selectivity is dose-dependent and is lost at high doses. They are preferred in patients with coexisting asthma, COPD, or peripheral vascular disease, although beta-blockers should still be used cautiously in severe airways disease.

What is the drug of choice for hypertensive emergency?

IV labetalol or nicardipine is preferred for most hypertensive emergencies. Sodium nitroprusside is used for severe acute hypertension, especially aortic dissection (combined with esmolol for heart-rate control), but cyanide toxicity limits use beyond 48 to 72 hours and in renal failure. Esmolol is the first choice for perioperative hypertension and aortic dissection.

Why does ACE inhibitor cause cough?

ACE inhibitors block the breakdown of bradykinin and substance P in the lung, leading to a dry, persistent cough in 5 to 20 percent of patients. The cough is not dose-related and can appear weeks to months after starting therapy. Switch to an ARB if the cough is troublesome, since ARBs do not affect bradykinin metabolism.

What antihypertensive is first-line in CKD with proteinuria?

ACE inhibitors or ARBs are first-line in CKD with proteinuria because they reduce intraglomerular pressure by efferent arteriolar dilation, slow proteinuria, and delay progression to end-stage renal disease. They are contraindicated in bilateral renal artery stenosis. Monitor potassium and creatinine within one to two weeks of starting; a creatinine rise above 30 percent demands stopping the drug.

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Written by: NEETPGAI Editorial Team Reviewed by: Pending SME Review Last reviewed: May 2026