Mechanism of glomerular permeability reduction in nonclipped kidney of rats with goldblatt hypertension

Glomerular hemodynamics were studied by micropuncture in undipped kidney of rats with two-kidney, one clip (2K1C) Goldblatt hypertension and in normotensive controls 30 to 45 days after placing the clip. Studies were performed before and after administration of captopril, 1 mg + 3 mg/kg/hr (7 control, 9 2K1C rats), and before and after infusion of hyperoncotic plasma, 15 g/dl, 1% of body weight (7 control, 7 2K1C rats). Morphological studies were performed in 20 rats to measure glomerular volume. High blood pressure increased glomerular pressure in spite of a rise in afferent resistance of more than 100%; glomerular filtration rate remained unchanged; and ultrafiltration coefficient decreased. After captopril, glomerular filtration rate increased 55% in normotensive controls and fell 11 % in 2K1C hypertensive rats. Glomerular pressure decreased 16% in hypertensive rats only; ultrafiltration coefficient increased in normotensive and hypertensive rats. Hyperoncotic plasma produced renal vasodilatation in both groups. Glomerular filtration rate rose 98% in normotensive rats and 15% in hypertensive rats. Glomerular pressure was elevated in both groups, but ultrafiltration coefficient increased only in the normotensive controls (48%), decreasing 6% in the hypertensive rats. Morphological studies showed dilatation of capillary loops and increased glomerular volume, which was directly related to systemic blood pressure (r = 0.79). The responses to captopril show that the contribution of angiotensin was similar in both groups. Therefore, angiotensin cannot be the main factor in reducing ultrafiltration coefficient in hypertensive rats. Lack of response to hyperoncotic plasma in hypertensive rats in spite of a rise in glomerular pressure suggests a predominant role of structural changes; enlarged glomeruli with low filtration rate denote decreased permeability of capillary wall.