The behaviour of blood pressure, sodium balance, plasma potassium, urinary and plasma aldosterone, plasma cortisol, growth hormone, 17 OH ketogenic steroids were studied in 20 mild hypertensive in-patients (10 with low and 10 with normal PRA) before, 1 day and 5 days after clonidine. Blood pressure was significantly decreased by clonidine while PRA was as a mean unchanged. No correlation was found between blood pressure changes and either basal PRA or aldosterone values or PRA and aldosterone changes after clonidine. Urinary aldosterone was significantly decreased by clonidine and aldosterone changes were unrelated to those parameters (PRA, plasma potassium, sodium balance, ACTH) which are known to influence aldosterone secretion, while GH showed a small increment the first day but was unchanged the fifth day. Plasma aldosterone was not significantly changed by clonidine but its changes showed an inverse correlation to urinary aldosterone changes. Conclusions: In our normal and low renin patients the antihypertensive action of clonidine is neither predicted by basal PRA and urinary aldosterone values nor explained by their changes. The opposite effect of clonidine on urinary aldosterone and plasma aldosterone may point to a decrease of metabolic clearance rate of the hormone exerted by the drug.

The effect of clonidine on renin and aldosterone of hypertensive patients.

PEDRINELLI, ROBERTO;
1980

Abstract

The behaviour of blood pressure, sodium balance, plasma potassium, urinary and plasma aldosterone, plasma cortisol, growth hormone, 17 OH ketogenic steroids were studied in 20 mild hypertensive in-patients (10 with low and 10 with normal PRA) before, 1 day and 5 days after clonidine. Blood pressure was significantly decreased by clonidine while PRA was as a mean unchanged. No correlation was found between blood pressure changes and either basal PRA or aldosterone values or PRA and aldosterone changes after clonidine. Urinary aldosterone was significantly decreased by clonidine and aldosterone changes were unrelated to those parameters (PRA, plasma potassium, sodium balance, ACTH) which are known to influence aldosterone secretion, while GH showed a small increment the first day but was unchanged the fifth day. Plasma aldosterone was not significantly changed by clonidine but its changes showed an inverse correlation to urinary aldosterone changes. Conclusions: In our normal and low renin patients the antihypertensive action of clonidine is neither predicted by basal PRA and urinary aldosterone values nor explained by their changes. The opposite effect of clonidine on urinary aldosterone and plasma aldosterone may point to a decrease of metabolic clearance rate of the hormone exerted by the drug.
Salvetti, A; Pedrinelli, Roberto; Cavasinni, L; Simonini, N.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11568/209134
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