Angiotensin II potentiates the arterial pressure response to volume loading in humans

Angiotensin II (AII) has many potential effects on blood pressure regulation in addition to direct vasoconstriction. This study tested the hypothesis that minimally pressor infusions of AII, which themselves exert minimal effects on blood pressure, might significantly perturb the pressure response to hypertonic volume expansion in healthy humans. Accordingly, 3% saline was infused at 0.1 mL/kg/min in 13 healthy volunteers, both with and without concomitant All infusion (2 ng/kg/min) on separate days. On a third day, All was infused alone for 2 h in eight of these subjects. Eight subjects also were studied with 3% saline plus concomitant phenylephrine infusion as a “positive control.” All and phenylephrine exerted similar, small effects on mean arterial pressure (3.3 ± 1.5 υ 3.0 ± 1.0 mm Hg, P = NS) before the infusion of AII When 3% saline was infused alone, mean arterial pressure did not rise significantly. In the presence of AII, mean arterial pressure rose from 89 ± 10 to 97 ± 11 mm Hg (P <.01 v control; P <.05 υ 3% saline alone). In the presence of phenylephrine, the mean arterial pressure did not increase during 3% saline infusion, similar to the results during 3% saline infusion alone. Plasma osmolality and arginine vasopressin levels were not different during 3% saline infusions with and without AII or with phenylephrine. Thus, a minimally pressor infusion of AII significantly potentiated the response of mean arterial pressure to hypertonic volume expansion in healthy humans. Many potential explanations are possible, but the phenylephrine experiments and arginine vasopressin responses make a nonspecific effect of concomitant pressor infusion or an effect of arginine vasopressin unlikely. These results may have implications for the pathogenetic role of AII in diseases such as hypertension and congestive heart failure. Am J Hypertens 1994;7:767–771.