Role of renin and aldosterone suppression in the antihypertensive mechanism of clonidine

• Published in: The American journal of medicine Vol. 65; no. 4; pp. 614 - 618
• Main Authors: Niarchos, Andreas P., Baer, Leslie, Radichevich, Ildico
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.10.1978
• Subjects: Adult; Aged; Aldosterone - metabolism; Angiotensin II - antagonists & inhibitors; Antihypertensive Agents; Blood Pressure - drug effects; Clonidine - pharmacology; Clonidine - therapeutic use; Female; Humans; Hypertension - drug therapy; Hypertension - enzymology; Hypertension - physiopathology; Male; Middle Aged; Renin - blood; Saralasin - pharmacology
• ISSN: 0002-9343; 1555-7162
• DOI: 10.1016/0002-9343(78)90849-5

The hypothesis that clonidine decreases blood pressure by suppression of the renin-angiotensin II-aldosterone system was investigated in 20 hypertensive patients during a constant sodium and potassium intake. A significant decrease in mean arterial pressure (MAP), from 123 ± 3 to 102 ± 3 mm Hg (P < 0.001) was observed in 15 patients (responders) during treatment with clonidine. In these patients, plasma renin activity (PRA) was decreased by clonidine from 9.9 ± 3.9 to 5.4 ± 1.6 ng/ml/hour (P < 0.05). The decrease in MAP correlated with the decrease in PRA (r = 0.685, P < 0.02) and with the pretreatment PRA (R = 0.596, P < 0.05). The aldosterone excretion was decreased by clonidine by 29 per cent (from 16 ±4 to 11 ± 2 μg/24 hours), but not significantly. However, the changes in PRA were significantly correlated with the changes in aldosterone (r = 0.645, P < 0.05). Among the responders to clonidine, those with the higher pretreatment PRA levels showed the greatest fall in blood pressure. A common characteristic of the nonresponders to clonidine (five patients) was the presence of moderate to severe renal insufficiency. Moreover, in the nonresponders, PRA and urinary aldosterone were not significantly suppressed by clonidine. In order to evaluate further the role of renin suppression as an antihypertensive mechanism during clonidine treatment, the renin (angiotensin II) dependency of hypertension was tested prior to the administration of clonidine by giving an infusion of the angiotensin II competitive antagonist, saralasln to eight patients. In four of the eight patients blood pressure was decreased by both clonidine and saralasin, whereas in three patients clonidine decreased MAP, but saralasin elicited a pressor response. Finally one nonresponder to clonidine exhibited a depressor response to saralasin. Thus, clonidine decreased blood pressure in patients with nonrenin-dependent hypertension. Over-all results indicate that although the decrease in blood pressure is related to renin suppression during treatment with clonidine, another antihypertensive mechanism (or mechanisms) still exists in hypertension without renin dependency.