Clearance and micropuncture studies were conducted on 6-wk-old spontaneously hypertensive rats (SHR) of the Okamoto-Aoki strain and normotensive Wistar-Kyoto rats (WKY) under euvolemic conditions. Mean arterial pressure in SHR was elevated by 18 mmHg and their kidneys were vasoconstricted with reduced blood flow; resistances in preglomerular vessels and efferent arterioles were elevated 2.8 and 2 times, respectively, above WKY values. Whole kidney glomerular filtration rate (GFR) and single nephron glomerular filtration rate (SNGFR), based on fluid collection from either proximal or distal convolutions, were 25-30% lower in SHR. Fractional reabsorptions of fluid load by the proximal convoluted tubule (43%) and by the loop of Henle (52-55%) were similar in both groups. Accordingly, SHR exhibited less fluid delivery from the proximal convolution (8 vs. 12 nl/min) and to the distal convolution (3 vs. 5 nl/min). Glomerular dynamics in hypertensive and normotensive strains were characterized by filtration pressure disequilibrium. Estimated glomerular capillary pressure and mean effective ultrafiltration pressure were similar in SHR and WKY. SHR had a lower glomerular ultrafiltration coefficient than WKY (0.011 vs. 0.016 nl X s-1 X mmHg-1), which, combined with a lower glomerular plasma flow (41 vs. 73 nl/min), quantitatively accounted for the lower SNGFR in 6-wk-old SHR. These findings document important differences in renal function in young SHR compared with WKY that may participate in the development of hypertension.
Tubular microperfusion was used to evaluate tubuloglomerular feedback (TGF)-mediated changes in single nephron glomerular filtration rate (SNGFR) and stop-flow pressure (SFP) in euvolemic 6- and 11- to 14-wk-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Young SHR compared with WKY had an elevated mean arterial pressure (107 vs. 90 mmHg, P less than 0.001) and a lower proximally measured SNGFR (14 vs. 17 nl/min, P less than 0.001) with no loop perfusion. Perfusion at 32 nl/min produced a greater decrease in SNGFR of SHR (6 vs. 2 nl/min, P less than 0.001). Although basal SFPs were identical (39 mmHg), loop perfusion elicited a greater maximal decline in SFP (-10 vs. -4 mmHg, P less than 0.001) and reactivity of SFP (-1.2 vs. -0.5 mmHg X min X nl-1, P less than 0.001) in young SHR; a lower rate produced a half-maximal decrease in SFP (7 vs. 10 nl/min, P less than 0.02). In adult rats, SNGFRs with no flow through Henle's loop were the same (27 and 28 nl/min) and perfusion at 32 nl/min produced similar decrements in SNGFR (-13 vs. -11 nl/min). The maximal change in SFP was greater in adult SHR (-12 vs. -10 mmHg, P less than 0.02), but there were no strain differences in maximal SFP reactivity (-1.8 vs. -1.3 mmHg X min X nl-1) and the rate eliciting half-maximal SFP changes (12 vs. 12 nl/min). Reduction of arterial pressure to the normotensive range did not alter responses in either age group of SHR.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of unilateral partial renal venous ligation on whole kidney and single nephron function were determined in anesthetized euvolemic Munich-Wistar rats using clearance, blood flow, and micropuncture techniques. Increased venous pressure (4-22 mmHg) reduced glomerular filtration rate (GFR) and renal plasma flow (RPF) to 60% of control values; filtration fraction (FF) was constant. Similar responses occurred in the superficial cortex, as evidenced by a 40% fall in SNGFR determined while intratubular pressure was maintained at the elevated precollection level. Fractional reabsorption by the proximal convoluted tubule remained constant, indicating maintenance of glomerulotubular balance. The contralateral kidney exhibit a diuresis and natriuresis while GFR and RPF were stable. In the experimental kidney single nephron glomerular plasma flow decreased by 35% due to increments in preglomerular and efferent arteriolar resistance. The transcapillary hydrostatic pressure gradient was unchanged since there were similar 7- to 8-mmHg increases in glomerular capillary and Bowman's space pressures. Filtration pressure disequilibrium was observed in control and experimental periods. Mean effective ultrafiltration pressure was similar in both periods. Specific values for the ultrafiltration coefficient (Kf) fell from 0.023 to 0.015 nl . s-1. mmHg-1. Accordingly, partial renal venous ligation produces ipsilateral vasoconstriction and a fall in GFR that is primarily due to a proportional decline in Kf.
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