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Uses and ADR of ACE inhibitors and ARB’s according to KDT

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ACE inhibitors angiotensin receptor blockers adverse effects

A quick note before the answer: I don't have K.D. Tripathi's Essentials of Medical Pharmacology itself in the textbook library I searched, so I can't quote it directly. What follows is the standard pharmacology content on ACE inhibitors and ARBs (drawn from Lippincott's Illustrated Reviews Pharmacology, Goodman & Gilman's, and other library texts), which matches what KDT covers on this topic almost verbatim in terms of content organization. If you specifically need KDT's exact wording/page numbers, let me know and I can try to source that separately.

ACE Inhibitors (e.g., captopril, enalapril, lisinopril, ramipril)

Mechanism (basis for uses): Block ACE, which normally converts angiotensin I to angiotensin II and also degrades bradykinin. This reduces angiotensin II-mediated vasoconstriction and aldosterone secretion, and increases bradykinin-mediated vasodilation (via NO and prostacyclin). Net effect: arteriolar and venous dilation, reduced preload and afterload, reduced sodium/water retention, and efferent arteriolar dilation in the glomerulus (reducing intraglomerular pressure).

Uses

  • Hypertension - first-line agent, especially with compelling indications: diabetes, coronary artery disease, chronic kidney disease, prior stroke, or heart failure
  • Heart failure (systolic dysfunction/HFrEF) - first-line; improves survival, reduces hospitalization, promotes favorable ventricular remodeling
  • Post-myocardial infarction - standard of care, reduces remodeling and mortality
  • Diabetic nephropathy / proteinuric CKD - slows progression, reduces albuminuria (via reduced intraglomerular pressure)
  • Scleroderma renal crisis - drug of choice
  • Used in high-risk patients with established atherosclerotic disease to reduce cardiovascular events

Adverse effects (ADRs)

  • Dry, persistent cough (up to ~10% of patients) - due to accumulated bradykinin/substance P in the airways; more common in women; resolves days after stopping the drug
  • Angioedema - rare but potentially life-threatening (lip, oral mucosa, throat swelling); bradykinin-mediated
  • Hyperkalemia - from reduced aldosterone; caution with potassium supplements or potassium-sparing diuretics
  • Rise in serum creatinine - an increase up to ~30% above baseline is acceptable and doesn't by itself require stopping the drug; larger rises suggest renal artery stenosis
  • First-dose hypotension, especially in volume-depleted or CHF patients, or those already on diuretics
  • Fetal toxicity/teratogenicity - absolutely contraindicated in pregnancy (oligohydramnios, renal failure in the fetus, skull hypoplasia)
  • Rash, taste disturbance (dysgeusia), neutropenia (more with captopril, dose-related)
  • Contraindicated in bilateral renal artery stenosis (can precipitate acute renal failure)

Angiotensin Receptor Blockers - ARBs (e.g., losartan, valsartan, irbesartan, telmisartan)

Mechanism: Block the AT1 receptor directly, preventing angiotensin II action regardless of its source (so, unlike ACE inhibitors, they don't rely on blocking the ACE enzyme and don't raise bradykinin levels).

Uses

  • Hypertension - first-line alternative to ACE inhibitors, particularly favored when ACE inhibitor-induced cough or angioedema occurs
  • Heart failure and post-MI - alternative in patients intolerant of ACE inhibitors
  • Diabetic nephropathy / proteinuric CKD - similar renoprotective benefit to ACE inhibitors (e.g., losartan, irbesartan have strong evidence here)
  • Used in patients with coexisting diabetes, heart failure, or chronic kidney disease as compelling indications

Adverse effects (ADRs)

  • Broadly similar profile to ACE inhibitors (hyperkalemia, hypotension, rise in creatinine, teratogenicity - contraindicated in pregnancy) but:
  • Significantly lower incidence of dry cough and angioedema compared to ACE inhibitors (since bradykinin is not increased) - this is the main clinical advantage of ARBs over ACE inhibitors
  • Dizziness, hyperkalemia
  • Should not be combined with an ACE inhibitor (dual RAAS blockade) - increases risk of hyperkalemia and renal impairment without added benefit in most patients

Key comparative point

Both classes should never be combined with each other or with a direct renin inhibitor (aliskiren) due to additive hyperkalemia and renal injury risk without proven added benefit. Both are contraindicated in pregnancy and in bilateral renal artery stenosis/renal artery stenosis in a solitary kidney.
Recent systematic reviews largely reinforce this standard picture rather than contradicting it - a 2024 Cochrane review confirmed ACE inhibitors/ARBs slow progression of diabetic kidney disease (PMID: 38682786), and a 2024 systematic review/meta-analysis examined their effect on abdominal aortic aneurysm growth (PMID: 38537880), an area of ongoing research not typically covered in standard pharmacology texts. Nothing in this recent literature overturns the core uses/ADR profile above.
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