Systemic and pulmonary hemodynamic effects of saralasin infusion in hypertension. Predictability of plasma renin status from hemodynamic changes.

Hemodynamic measurements were obtained before and after 30 minutes of saralasin infusion in 26 fasting adults with hypertension (25 men and 1 woman). Nine showed a depressor response with a decrease in mean intaarterial pressure greater than 20 mm Hg. Ten were nonresponders and seven had an agonistic response with an increase in mean arterial pressure of greater than 10 mm Hg. Heart rate, pulmonary arterial and wedge pressures and pulmonary vascular resistance were nearly identical in the three groups and remained unchanged. Cardiac index decreased from a mean of 2.76 +/- 0.14 (standard error of the mean) to 2.48 +/- 0.1 liters/min per m2 in the nonresponders (P less than 0.02) but remained unchanged in the groups with a depressor or an agonistic response. The mean systemic vascular resistance decreased from 2,406 +/- 303 to 1,839 +/- 265 dynes sec/cm5 in the group with a depressor response (P less than 0.001) and increased in nonresponders (less than 0.02) and those with an agonistic response (P less than 0.01). However, regardless of the response of mean arterial pressure, systemic vascular resistance decreased only in the 10 patients with a plasma renin activity greater than 5 ng/ml per hour (8 from the depressor response group and 1 each from the nonresponse and agonistic response groups). It is concluded that (1) classification based soley on the response of aterial pressure to saralasin ignores important hemodynamic changes; (2) the response of cardiac index--no change in the patients with a depressor response and a reduction in nonresponders--suggests that endogenous angiotension II supports cardiac output in these groups; (3) a decrease in systemic vascular resistance is better than a decrease in mean arteiral pressure as a predictor of the status of the plasma renin activity; and (4) lack of change in pulmonary vascular resistance suggests that endogenous angiotension II plays an insignificant role in maintaining the resistance of the pulmonary vasculature.