The present study assessed the contribution of the renin-angiotensin system (RAS),
dietary sodium, and cardiac output (CO) to the genesis of primate
hypertensin 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 less than 0.0005), associated with increased plasma
renin activity (PRA) from 4.9 +/- 0.7 to 13.8 +/- 1.1 ng. ml-1.hr-1 (p less than 0.0005). Correlation of MAP with PRA yielded an r value of 0.662 (p less than 0.0005). Significant blood pressure elevation was obtained with both regular (R) and low
sodium (LS) diet (p less than 0.0005), although the MAP change was greater with LS. With both R and LS diet,
hypertension was associated with increased PRA (p less than 0.0005), and normotensive pressures were achieved with converting
enzyme inhibitor (
teprotide). 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 less than 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.