REVIEW

Renin: friend or foe?

Morris J Brown

Correspondence to:
Professor M Brown
Clinical Pharmacology Unit, Box 110, Addenbrookes Hospital, Cambridge CB2 2QQ, UK; m.j.brown{at}cai.cam.ac.uk

Renin maintains blood pressure through vasoconstriction when there is inadequate salt to maintain volume. In populations where blood pressure is more often high than low, and vascular death more common than haemorrhage or dehydration, therapeutic reductions in renin secretion or response are valuable. Whether long-term benefits are due entirely to blood pressure reduction remains unproved. The pathway can be blocked at its rate-limiting step (ß blockade or direct renin inhibition), the synthesis of the active product, angiotensin II, or at the receptor for angiotensin. Because renin and sodium are the two main factors in blood pressure control, and renin levels vary inversely with sodium load, blood pressure control requires a combination of natriuresis and blocking the consequential increase in renin activity. Being a large and stable molecule, renin is among the easiest and cheapest of hormone measurements. Understanding the simple biochemistry and physiology of renin permits optimal use of the drugs acting to raise or suppress this hormone.

Abbreviations: ACEi, ACE inhibitor; Ang I (II), angiotensin I (II); ARBs, angiotensin receptor blockers; BP, blood pressure; CCBs, calcium channel blockers; DRI, direct renin inhibitor; JGA, juxtaglomerular apparatus; PRA, plasma renin activity; RAS, renin–angiotensin–aldosterone system

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