Relationship between plasma aldosterone and angiotensin II before and after noradrenergic inhibition in normal subjects and patients with mild essential hypertension.
The responsiveness of plasma aldosterone to the infusion of angiotensin II at dose rates of 2, 4, and 10 ng/kg X min was assessed in 11 normal subjects and 13 patients with mild essential hypertension before and after 4 weeks of treatment with the sympatholytic agent debrisoquine. Debrisoquine treatment caused a significant (P less than 0.01) decrease in circulating norepinephrine (-45%), but did not modify plasma levels of angiotensin II, renin, aldosterone, or epinephrine or the metabolism of sodium or potassium. In normal subjects, debrisoquine caused a significant shift to the left (P less than 0.05) of the correlation relating plasma aldosterone to plasma angiotensin II levels. In patients with essential hypertension, the aldosterone-angiotensin II interrelationship was not modified. These findings suggest that the sympathetic nervous system exerts an inhibitory influence on aldosterone responsiveness to angiotensin II in normal man, and that this physiological interaction is impaired in patients with essential hypertension.
D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood*; D000804:Angiotensin II / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D003647:Debrisoquin / Q000494:pharmacology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood*; D007263:Infusions, Parenteral; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000037:antagonists & inhibitors*
D000804:Angiotensin II; D000450:Aldosterone; D003647:Debrisoquin; D009638:Norepinephrine