Clinical meaning
ACE inhibitors and angiotensin receptor blockers target the renin-angiotensin-aldosterone system at different points with distinct clinical implications for NP prescribing. ACEIs (enalapril, lisinopril, ramipril) block the conversion of angiotensin I to angiotensin II and additionally inhibit the degradation of bradykinin (a vasodilator and mediator of cough and angioedema). ARBs (losartan, valsartan, candesartan, telmisartan) selectively block the AT1 receptor, preventing angiotensin II from exerting its effects (vasoconstriction, aldosterone secretion, sympathetic activation, cardiac remodeling) while preserving AT2 receptor-mediated beneficial effects (vasodilation, anti-proliferation). The clinician selects between these classes based on indication, evidence base, and adverse effect profile: ACEIs have stronger evidence for mortality reduction in heart failure (CONSENSUS, SOLVD trials) and post-MI (SAVE, AIRE trials), while ARBs are preferred when ACEI intolerance occurs (cough in 5-20% of patients due to bradykinin accumulation, more common in females and patients of East Asian descent). Both classes are first-line for diabetic nephropathy (reducing proteinuria through preferential efferent arteriolar dilation, decreasing intraglomerular pressure), hypertension in diabetes, and heart failure with reduced ejection fraction. Prescribing considerations include: monitoring serum potassium and creatinine 1-2 weeks after initiation or dose change (acceptable rise in creatinine up to 30% from baseline), avoiding concurrent use of ACEIs and ARBs (ONTARGET trial showed increased adverse effects without benefit), absolute contraindication in pregnancy (teratogenic -- fetal renal dysgenesis), and caution in bilateral renal artery stenosis (dependent on efferent arteriolar constriction to maintain GFR).