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Mechanisms of Hypertension during the Chronic Phase of the One‐Clip, Two‐Kidney Model in the Dog

The mechanism of the chronic phase of one-clip, two-kidney hypertension was investigated in 23 dogs. Mean arterial pressure (MAP), renal hemodynamics, and arterial and renal venous plasma rerun activity (PRA) were studied before and at 1 and 3 months after graded, unilateral renal artery constriction. In the dogs that demonstrated sustained hypertension, the magnitude of changes in MAP, renal hemodynamics, PRA, and renal renin secretion correlated with the severity of renal artery constriction. In dogs with severe constriction (group 3, 78-86% renal blood flow reduction), MAP and arterial PRA were significantly elevated throughout. In groups 1 and 2 (0% and 50-56% renal blood flow reduction, respectively), although MAP remained significantly elevated, arterial PRA decreased to baseline values by 3 months. In group 3, there was an initial, apparent redistribution of ipsilateral renal blood flow, and prolonged reductions in ipsilateral renal plasma flow (RPF) and glomerular filtration rate accompanied by significantly increased creatinine clearance (Ccreat) in the untouched kidney. Similar but less marked renal hemodynamic changes occurred in the other hypertensive dogs. All hypertensive dogs, regardless of degree of renal artery constriction, demonstrated significantly increased ipsilateral renal renin secretion and contralateral renin suppression. In three dogs that were studied 6,12, and 16 months postconstriction, the high rate of ipsilateral renin secretion persisted throughout. Ipsilateral nephrectomy consistently resulted in rapid amelioration of the hypertension. These findings are in accord with a renal-dependent and probably renin-mediated mechanism for the maintenance of high blood pressure in the chronic phase of the one-clip, two-kidney dog model.