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Keywords:

Adult, Angiotensin I, Angiotensin II, Blood Pressure, Captopril, Female, Heart Rate, Humans, Hypertension, Hypertension, Renal, Hypertension, Renovascular, Male, Peptidyl-Dipeptidase A, Proline, Renin, Saralasin, Science & Technology, Life Sciences & Biomedicine, Urology & Nephrology, 1103 Clinical Sciences, 3202 Clinical sciences

Abstract:

The effects of an angiotensin-II analog (saralasin, i.v.) and of a converting enzyme inhibitor (captopril, oral) were compared in 12 sodium-depleted patients with hypertension. The decrease of the mean intraarterial pressure (MAP) with captopril (-21.5 +/- [SEM] 4.3 mm Hg) was more pronounced (P < 0.001) than the change of MAP during saralasin (-10.5 +/- 4.0 mm Hg). The pretreatment arterial plasma renin activity (log PRA) was closely related to the change of MAP during saralasin (r = -0.94; P < 0.001) and also to the captopril-induced change of MAP (r = -0.82; P < 0.001); similar results were obtained for the log plasma angiotensin (PA) I and II levels. The change of MAP was more pronounced, however, with captopril than during saralasin at any level of pretreatment PRA, PAI or PAII. Saralasin did not affect heart rate (P > 0.4), but during captopril the heart rate increased by 5.1 beats/min (P < 0.001). Captopril produced a 70% decrease of PAII, but the change of MAP was poorly related to the changes of PAII (r = -0.57; P < 0.05); PRA and PAI rose threefold to fourfold. PRA, PAI, and PAII all increased during saralasin. These observations may suggest that the antihypertensive action of captopril is not based solely on the inhibition of AII formation, but also the agonistic effect of saralasin has to be considered.