The renin system and new understanding of the complications of hypertension and their treatment.
The renin-angiotensin-aldosterone hormonal axis is the major long-term servocontrol for regulation of both arterial blood pressure and sodium balance. It supports normotension or hypertension via angiotensin vasoconstriction and angiotensin plus aldosterone-induced renal sodium retention. Normally, in the presence of hypertension or sodium-volume excess, plasma renin activity promptly falls to zero. Accordingly, any renal secretion of renin in the face of high blood pressure is abnormal. In established essential hypertension varying degrees of abnormal plasma renin activity operate to cause or sustain the hypertension; only very low plasma renin values reflect a normal renal response. Human hypertensive disorders comprise a spectrum of abnormal plasma renin-sodium volume products. High renin, intensely vasoconstricted, hypovolemic forms (e.g., malignant, renovascular) are one extreme of the spectrum; "wet"-volume-excess low-renin forms are the other extreme (e.g., primary aldosteronism, low-renin essential hypertension). These varying, but abnormal renin-sodium products are caused by a renal lesion in which a subpopulation of ischemic nephrons hypersecretes renin and retains sodium despite systemic hypertension and sodium excess. Thus, hypertensive patients cannot suppress their renin secretion normally. The hypertension from this renal lesion is correctable by agents that reduce renin secretion or block its effect (beta blockade, CEI, renin inhibition, or angiotensin II antagonism). None of these agents lower blood pressure after binephrectomy, verifying the renal origin of renin in the cardiovascular control system. In essential hypertension, the plasma renin level appears as a continuous variable associated with greater risk of ischemic injury.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiovascular Center, New York Hospital, Cornell Medical Center, New York.
J H
JH
Laragh
D000818:Animals; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D012083:Renin / Q000502:physiology*
D012083:Renin