Renin–Angiotensin System in Mild Essential Hypertension.

Abstract

ABSTRACT. Twenty‐five 40‐year‐old patients with mild essential hypertension, identified during a survey of a population born in 1936, were investigated. Basal and postfurosemide values for plasma renin concentration (PRC) and plasma angiotensin II concentration (PA II) did not differ markedly from reference values measured in 40‐year‐old control subjects from the same population. In the untreated sodium replete state, saralasin infusion (5.4 nmol/kg/min) produced an increase in mean arterial pressure (MAP) in the patient group as a whole. Twenty‐one patients were treated with hydrochlorothiazide, mean dose 75 mg/day for 3 months, and the examinations were repeated in 20 patients. Pretreatment furosemide‐stimulated PRC and PA II, and values during thiazide treatment were higher in “non‐responders” to hydrochlorothiazide treatment (n=10) than in “thiazide reponders” (n=11). During thiazide therapy, angiotensin II blockade induced a clearcut decrease in MAP in every single “thiazide non‐responder”, whereas 7 out of 11 “thiazide responders” did not show any fall in BP, and 4 exhibited only a borderline decline in MAP. After thiazide and angiotensin II blockade, significant differences in MAP were no longer present between the two patient groups. It is concluded that in mild untreated essential hypertension, angiotensin II has no decisive role in the maintenance of high BP. The functional significance of the renin–angiotensin system (RAS) emerges after thiazide treatment. Thiazide‐induced stimulation of RAS coutnerbalances the hypotensive effect of thiazide in some 40% of the treated patients. Thus the responsiveness of RAS determines the quantitative BP response to treatment. Assessment of angiotensin II response to acute stimulation could to some extent predict the subsequent response to thiazide treatment. Saralasin infusion serves as a reliable tool for assessing the participation of angiotensin II in BP regulation.