CHANGES OF HEMODYNAMICS AND GLOMERULAR ULTRAFILTRATION IN RENAL-HYPERTENSION OF RATS

Determinants of glomerular ultrafiltration were studied by micropuncture in clamped (N=11) and unclamped (N=7) kidneys of two-kidney Goldblatt rats and compared to 15 controls. Renin-dependence of hypertension (184±9 [SD] mm Hg, 3 to 4 week's duration) was demonstrated by infusing the angiotensin-II-antagonist saralasin. In clamped kidney hydrostatic pressure in glomerular capillaries (P(GC)) was reduced to 56.5±3.0 vs. 61.2±3.4 mm Hg in controls, whereas renal perfusion pressure behind the clip was normal. Early proximal flow rate (EPFR) was decreased to 20.5±0.8 vs. 25.8±1.5 nl/min in controls, at an unchanged single nephron filtration fraction (SNFF), indicating a reduced glomerular plasma flow (SNGPF). Preglomerular vascular resistance (R(A)) was increased by 21%, but postglomerular resistance (R(E)) remained unchanged. In unclamped kidneys, P(GC) was increased to 65.0±1.9, and pressures in peritubular capillaries (P(C)) were increased to 17.5±1.6 mm Hg. P(C)/P(GC) ratios were significantly higher. EPFR was increased to 32.1±1.9 nl/min, indicating, at an unchanged SNFF, an increased SNGPF. R(A) increased by 51%, whereas R(E) declined by 25%. The ultrafiltration coefficient was reduced by 24% in unclamped kidneys. The number of glomeruli was lower in clamped (24,590±5,500) and was higher in unclamped kidneys (33,580±4,110) compared to controls (29,240±4,900). The authors' results indicate that in clamped kidneys an increase of R(A) causes a reduction of P(GC) and, hence, a reduction of pressure at the baroreceptor site which may be a trigger mechanism for renin release. In unclamped kidneys, adaptation of R(A) and R(E) to high perfusion pressure is nearly perfect, in terms of an active component of R(E) dilatation.