Role of the renin-angiotensin system in blood pressure regulation. The cardiovascular effects of converting enzyme inhibition in normotensive subjects.

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Abstract
The role of the renin-angiotensin system in the regulation of blood pressure in normal human subjects was investigated by administering to them the converting enzyme inhibitor [teprotide] (SQ 20881) during Na replete and Na depleted states. In the Na replete state (150 meq Na intake for 5 days) in 8 normal subjects, converting enzyme inhibitor decreased the average mean arterial pressure from 75 .+-. 4 to 65 .+-. 5 mm Hg (P < 0.005) because of a decrease in peripheral resistance from 17 .+-. 1 to 14 .+-. 1 U [units] (P < 0.025). Cardiac output did not change because of a simultaneous decrease in venous return. Na depletion (10 meq Na intake for 5 days) in 6 subjects resulted in an insignificant decrease in blood pressure (from 75 .+-. 4 to 69 .+-. 2 mm Hg), whereas cardiac output decreased from 5.15 .+-. 0.29 to 3.91 .+-. 0.22 l/min (P < 0.05). Plasma renin activity increased with Na depletion from 2.13 .+-. 0.38 to 7.3 ng/ml per h (P < 0.005). Converting enzyme inhibitor administration in the Na depleted state (n = 6) decreased mean arterial pressure from 69 .+-. 2 to 53 .+-. 5 mm Hg (P < 0.005) because of a decrease in peripheral resistance from 18 .+-. 1 to 12 .+-. 1 U (P < 0.005), whereas cardiac output increased from 3.91 .+-. 0.33 to 4.40 .+-. 0.30 l/min (P < 0.005). The maximum decrease in diastolic blood pressure caused by the inhibitor correlated to the control plasma renin activity (r [correlation coefficient] = 0.76, P < 0.01, n = 14 measurements). The renin-angiotensin system apparently participates in the regulation of blood pressure and cardiac function in normal subjects, even in the Na-replete state. This role of the renin-angiotensin system in cardiovascular homeostasis in normal subjects becomes more crucial during Na depletion when plasma renin (angiotensin II) is markedly increased.