The purpose of the present study was to characterize the etiology of bilateral
perinephritis hypertension in the non-human primate.
Hypertension was induced in female cynomolgus (Macaca fascicularis) monkeys by wrapping both kidneys under sterile
surgical procedures. Mean arterial pressure (MAP), plasma
renin activity (PRA), plasma
aldosterone concentration (ALDO), para-aminohippurate (PAH) clearance, glomerular filtration rate (GFR), urine volume, and
sodium and
potassium excretion were measured before and weekly after induction of the
hypertension. MAP increased progressively from 108 +/- 1 to 135 +/- 4 mmHg during the first 6 weeks; thereafter, MAP remained at this elevated level, PRA was elevated two- to fivefold for up to 10 weeks after the
hypertension and ALDO was elevated during 1 (139%), 4 (60%), 6 (196%), 8 (249%) and 10 (148%) weeks of the
hypertension. PAH clearance and GFR were significantly reduced during week 1 of the
hypertension, but returned to control values by week 2. Urine volume was increased significantly during the first week of the
hypertension, while
sodium and
potassium excretion were not changed.
Captopril (15 mumol/kg, intravenously) normalized the blood pressure regardless of the severity or duration of the disease. Additionally,
captopril lowered ALDO and increased PRA. It is concluded that bilateral
perinephritis hypertension in the monkey is dependent on increased activity of the
renin-
angiotensin-
aldosterone axis.