Adrenergic activity and aldosterone regulation: no evidence for an alpha-1 adrenoceptor-mediated influence in normal subjects.
In normal man the sympathetic nervous system could exert an inhibitory influence on aldosterone responsiveness to angiotensin II. The possible role of alpha-1 adrenoceptors in the modulation of aldosterone response was assessed by studying the changes of plasma aldosterone during infusion of angiotensin II at the doses of 1, 2, 5 and 10 ng/kg.min or after corticotrophin injection, 0.25 mg, in 9 normal subjects before and after treatment with the selective alpha-1 adrenoceptor antagonist, prazosin. Prazosin, given during 3 weeks, did not modify supine arterial pressure, heart rate and the plasma levels of angiotensin II, renin, aldosterone or adrenaline but caused a significant (P less than 0.05) increase of plasma noradrenaline. The correlation relating plasma aldosterone to plasma angiotensin II levels before and during angiotensin II infusion and the response of plasma aldosterone to corticotrophin was not modified by prazosin. These findings suggest that in normal man there is no inhibitory influence of the noradrenergic system on aldosterone responsiveness to angiotensin II mediated by an alpha-1 dependent mechanism.
D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000328:Adult; D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000494:pharmacology*; D003864:Depression, Chemical; D006801:Humans; D008297:Male; D009638:Norepinephrine / Q000097:blood; D011224:Prazosin / Q000494:pharmacology; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects / Q000502:physiology*
D011942:Receptors, Adrenergic, alpha; D000804:Angiotensin II; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D009638:Norepinephrine; D011224:Prazosin