Role of renin secretion and kidney function in hypertension and attendant heart attack and stroke.

Abstract

Control of blood pressure usually has not, by itself, affected the incidence of heart attack in hypertensive patients. This suggests a need for cause-specific therapy targeted against mechanisms that engage the risks of myocardial infarction. Study of the renin system, the ongoing, long-term servo-control over blood pressure and electrolyte homeostasis may provide answers. Inappropriately high renin production, generating the powerful vasoconstrictor, angiotensin II, may cause ischemic vascular damage in the heart, kidney and brain, predisposing to infarction. Many clinical situations associated with high plasma renin levels are accompanied by striking vascular damage, heart attack, or stroke. A recent prospective study of 1,717 hypertensive patients shows an unequivocally positive relationship between myocardial infarction and high-renin status regardless of other risk factors such as smoking, hypercholesteremia, or diabetes. The data also suggest the possibility that renin is a continuous variable, since the risk of heart attack was significantly weaker in medium-renin than in high and significantly greater than in low renin subjects. These observations are in keeping with concept that any renin secretion in the face of arterial hypertension is abnormal, since the truly normal kidney completely turns off its renin secretion. Thus the renin-sodium profile appears to be especially useful for evaluating the large fraction of patients who develop heart attacks in the absence of these other risk factors. Although, these findings suggest that a renin test should be performed routinely in hypertensive patients, the better to assess prognosis and design appropriate anti-renin therapy.