• The main physiological role of the renin angiotensin system (RAS) is to protect against Na+ loss, and the hypotension which results. When inappropriately high for the level of Na+ in the body, renin production can contribute to hypertension and end-organ damage.
• Renin secretion is regulated by four mechanisms: arterial pressure, sympathetic nervous system activity, salt intake and negative feedback regulation by Ang II.
• Most antihypertensive medications influence the measurement of plasma renin activity (PRA), acting on one of the above mechanisms. ACE inhibitors, ARBs, CCBs and diuretics increase PRA, whereas beta-blockers and renin inhibitors reduce PRA.
• At the population level, PRA is negatively correlated with age and Na+ intake, and therefore also with blood pressure. In many patients with hypertension, however, PRA is inappropriately high for the level of Na+ intake, and limits the effectiveness of drugs used to eliminate Na+.
• In hypertension, therefore, it is rational to combine drugs which, respectively, eliminate Na+ and block the RAS. Combination treatment is likely to become routine even for initial treatment of most patients, and will improve rates of BP control.
• In high-renin states, namely heart failure, strategies to increase RAS suppression (e.g. ACE inhibitor/ARB combination therapy) can improve treatment outcomes. In other conditions, benefits are proportional to the prior contribution of renin to a patient’s hypertension or other cardiovascular risk.
• Measurement of renin is now straightforward. In addition to diagnosis of secondary causes of hypertension, the measurement permits recognition and titration of the low-renin patient in whom extra diuretic is required to de-suppress renin secretion and potentiate further RAS blockade.
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