Acute Hypertension in a Nonhuman Primate: Humoral and Hemodynamic Mechanisms

The present study assessed the contribution of the renin-angiotensln system (RAS), dietary sodium, and cardiac output (CO) to the genesis of primate hypertension in a one-kidney model which was developed to test species-specific renin inhibitors. Reduction of renal perfusion pressure increased mean arterial pressure (MAP) from 105 ± 4 to 127 ± 3 mm Hg (p < 0.0005), associated with increased plasma renin activity (PRA) from 4.9 ± 0.7 to 13.8 db 1.1 ng.mlhr (p < 0.0005). Correlation of MAP with PRA yielded an r value of 0.662 (p < 0.0005). Significant blood pressure elevation was obtained with both regular (R) and low sodium (LS) diet (p < 0.0005), although the MAP change was greater with LS. With both R and LS diet, hypertension was associated with increased PRA (p < 0.0005), and normotensive pressures were achieved with converting enzyme inhibitor (teprodde). The hemodynamic change with hypertension was an increase of systemic vascular resistance (SVR) from 0.89 ± 0.12 to 1.17 ± 0.09 units {p < 0.05); cardiac output (CO) and central blood volume did not change significantly. Thus, acute hypertension, mediated by the RAS, was developed in a one-kidney primate model. The hemodynamic correlate of hypertension was increased SVR; CO and volume redistribution were not Initiating factors. (Hypertension 4219–225, 1982)