Hemodynamic mechanism of blood pressure response to captopril in human malignant hypertension.

Abstract

The hemodynamic mechanism of blood pressure response to angiotensin blockade is well established in "benign" but not in human malignant hypertension. We studied the changes in mean arterial pressure (MAP), cardiac index (CI), pulmonary wedge pressure (PWP), and in plasma volume (PV) induced by a single oral dose of captopril (150 mg) in 11 patients with malignant hypertension. Two hours after captopril, MAP fell from 178.5 +/- 5.8 to 151.8 +/- 7.8 mm Hg (p less than 0.001) (means +/- SEM) due to a fall in total peripheral resistance (TPR) (from 54.8 +/- 6.8 to 46.4 +/- 1.6 arbitrary units, p less than 0.001). However, there was a simultaneous increase in CI (from 3.29 +/- 0.13 to 3.70 +/- 0.15 liter/min/m2, p less than 0.001), and a decrease in PWP (from 15.3 +/- 3.5 to 11.0 +/- 2.5 mm Hg, p less than 0.001), while PV remained unchanged (from 4.02 +/- 0.26 to 4.12 +/- 0.12 liters, n.s.). Our data show that, in human malignant hypertension, blood pressure response to captopril is due to a decrease in TPR, but in contrast to benign hypertension, there is also a simultaneous increase in CI. Our results suggest that, in malignant hypertension, potentially high CI levels are artificially normalized by the increased TPR and may be fully disclosed by vasodilation.