Single-nephron hemodynamics in one-kidney one-clip hypertension in the rat.

Determinants of glomerular ultrafiltration were studied by micropuncture in clamped kidneys of one-kidney Goldblatt rats (n = 10, mean arterial pressure (MAP) = 183 +/- 18 (SD) mm Hg) and in control kidneys of unilateral nephrectomized rats (n = 14, MAP=120 +/- 14 mm Hg). Following saralasin infusion, no significant MAP change occurred in either group. Renal perfusion pressure of clamped kidneys (115 +/- 13 mm Hg) was not different from MAP in controls. Hydrostatic pressure in glomerular capillaries in clamped kidneys was not different from that in controls (60.9 +/- 2.1 vs. 61.7 +/- 3.5 mm Hg). Early proximal flow rate, as a measure for single-nephron GFR, was decreased to 29.5 +/- 1.5 vs. 36.6 +/- 4.4 nl/min in controls (p less than 0.01). Total renal resistance was increased by 102% in the hypertensive group, mainly due to the stenosis (75%) rather than the renal vasculature (27%). Due to a predominant increase of postglomerular vascular resistance, filtration fraction was increased in clamped kidneys (0.37 +/- 0.05 vs. 0.34 +/- 0.06, p less than 0.001). Single nephron glomerular plasma flow was decreased to 158 +/- 23.5 vs. 209 +/- 45.1 nl/min in controls (p less than 0.001). Efferent net ultrafiltration pressure did not differ significantly from zero in either group, i.e. filtration equilibrium was achieved. These results indicate an increased vascular resistance in clamped kidneys, which is caused by a preferential efferent vasoconstriction. This pattern of the vascular bed helps to prevent a further reduction of GFR despite a decrease of blood flow.

Goldblatt hypertension in rats: a model for unilateral renal artery stenosis in man.

Determinants of glomerular ultrafiltration were studied by micropuncture in clamped (n = 11) and unclamped (n = 7) kidneys of two-kidney hypertensive rats and compared to 15 controls. Infusion of the angiotensin II antagonist and saralasin lowered the blood pressure significantly. Glomerular capillary pressure (PGC) in clamped kidneys was decreased to 56 +/- (SD) 3 vs. 61 +/- 3 mm Hg in controls. Early proximal flow rate (EPFR) was decreased to 20 +/- 1 vs. 26 +/- 2 nl/min in controls, at an unchanged single nephron filtration fraction (SNFF), indicating a reduced glomerular plasma flow (SNGPF). Preglomerular resistance (RA) was increased by 21%. In unclamped kidneys PGC was increased to 65 +/- 2 mm Hg. EPFR was increased to 32 +/- 2 nl/min, indicating, at an unchanged SNFF, an increased SNGPF. RA increased by 51%, whereas postglomerular resistance declined by 25%. The ultrafiltration coefficient was reduced by 24% in unclamped kidneys. Our results indicate that in clamped kidneys an increase of RA causes a reduction of PGC and hence a reduction of pressure at the baroreceptor site which may act as a trigger mechanism for renin release.

[Effect of high-dosage prednisolone administration on interstitial transplantation edema following allogeneic kidney transplantation in rats]. / Einfluss der hochdosierten Prednisolonverabreichung auf das interstitielle Transplantatödem nach allogener Ratten-Nierentransplantation.

To measure subcapsular pressure of rat kidneys and kidney allografts, microcatheters were implanted in the subcapsular space and the pressure was continuously recorded with a transducer. Subcapsular pressure was found to increase significantly during allograft rejection. After single bolus injection of prednisolone 300 mg/kg on the day of transplantation or on the fourth postoperative day, considerably lower subcapsular pressures were recorded. This steroid effect together with other immunosuppressive measures could have an important influence on graft function and prognosis.

Single nephron filtration, luminal flow and tubular fluid reabsorption along the proximal convolution and the pars recta of the rat kidney as influenced by luminal pressure changes.

Intratubular pressures were measured in free flow and after blockade of tubular flow at different distances from the glomerulum in the kidney of Wistar rats. Free flow pressure was ffp = 13.3 +/- 2.5 Torr and stop flow pressure sfp = 41.7 +/- 3.8 Torr. With increasing distance of the blockade from the glomerulum the intratubular pressure decreased being 22.4 +/- 2.1 Torr, when the tubule was blocked at the end of the pars recta. In a second series single nephron filtration rate (gfr) and late proximal flow rates (V) were measured at different intratubular pressures. Free flow gfrf was 26.5 +/- 5.9 nl/min and Vf = 14.7 +/- 4.0 nl/min. The difference of these flow rates divided by tubular length results in a local reabsorption rate of C = 2.9 +/- 0.9 nl/min-mm in the proximal convolution. In the pars recta local reabsorbtion rate was 1.0 +/- 0.3 nl/min-mm. In the proximal convolution C increased with increasing intratubular pressure: deltaC/deltaitp = (2.7 +/- 1.2)-10(-2) nl/min-mm-Torr. Filtration was in disequilibrium in these animals under all conditions examined, hydraulic filtration conductance was K = 1.2 +/- 0.4 nl/min-Torr. Modified methods have been used for intratubular pressure and for flow rate measurements in order to reduce experimental procedure. It is shown, that fractional reabsorption, calculated on the basis of pressure measurements, is a good approximation to results usually obtained by inulin measurements.