Effects of angiotensin antagonism on hemodynamics, renin, and catecholamines during exercise

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Abstract
Oxygen uptake (.ovrhdot.VO2), mean intraarterial pressure (P), heart rate (HR), cardiac index (CI), stroke index (SI), total peripheral resistance index (TPRI), and plasma renin activity (PRA), norepinephrine (PNE), epinephrine (PE) and plasma lactate (PL) were estimated in 6 normotensive male subjects during rest in recumbency and during i.v. infusion of either glucose or saralasin in recumbent position, sitting position on the ergometer bicycle, and during submaximal graded exercise. .ovrhdot.VO2 was not different between the tests during glucose and during saralasin. At rest recumbent and in the sitting position .hivin.P, HR, CI, SI, and TPRI were not significantly different between both series of tests. During exercise, these variables increased to the same extent. From 110 W on, the increase in .hivin.P was significantly lower during saralasin as compared to glucose, and TPRI was significantly lower during saralasin at the final work load. In recumbency, saralasin did not cause changes in PRA, PNE and PE. In the sitting position, PRA tended to increase, while PNE doubled and PE remained unchanged in both series. Physical exercise produced exponential increases in PRA, PNE, PE and PL. The rises in PNE and PE were similar in both series, except that PNE was significantly lower at the final work load during saralasin. These observations suggest that the higher plasma angiotensin II levels during physical exercise increase TPRI and .hivin.P both by direct arteriolar vasoconstriction and by facilitating the release of NE at adrenergic nerve endings.

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