Pelayo J C, Blantz R C
Am J Physiol. 1984 Jan;246(1 Pt 2):F87-95. doi: 10.1152/ajprenal.1984.246.1.F87.
Nephron filtration rate (SNGFR), its determinants, and proximal tubular reabsorption were measured in hydropenic Munich-Wistar rats with sham-operated (sham) or denervated (DNx) kidneys before and during the administration of [Sar1, Ala8]angiotensin II or SQ 14225. The glomerular ultrafiltration coefficient (LpA) was significantly lower in DNx than in sham rats (P less than 0.025). However, SNGFR was not altered due to an offsetting increment in transcapillary glomerular hydrostatic pressure (delta P) in DNx (P less than 0.005). The marked increment of delta P in DNx was due to an increase in the glomerular capillary hydrostatic pressure, secondary to decreased afferent arteriolar resistance. The infusion of angiotensin II inhibitors to denervated kidneys completely normalized LpA but did not alter sham values. SQ 14225 but not [Sar1, Ala8]angiotensin II infusion provided a nephron plasma flow-dependent increase in SNGFR, secondary to a striking reduction in both glomerular vascular resistances. Endogenous angiotensin II activity may be enhanced by renal denervation, and angiotensin II acts to reduce LpA in this condition and may modulate the final level of renal vascular resistances after acute renal denervation.
在禁水的慕尼黑-维斯塔尔大鼠中,于假手术(假手术组)或去神经支配(去神经组)的肾脏给药[Sar1, Ala8]血管紧张素II或SQ 14225之前及期间,测量了肾单位滤过率(SNGFR)、其决定因素以及近端肾小管重吸收。去神经组的肾小球超滤系数(LpA)显著低于假手术组大鼠(P < 0.025)。然而,由于去神经组跨毛细血管肾小球静水压力(ΔP)的抵消性增加,SNGFR未发生改变(P < 0.005)。去神经组ΔP的显著增加是由于肾小球毛细血管静水压力升高,这继发于入球小动脉阻力降低。向去神经支配的肾脏输注血管紧张素II抑制剂可使LpA完全恢复正常,但未改变假手术组的值。输注SQ 14225而非[Sar1, Ala8]血管紧张素II可使SNGFR依肾单位血浆流量增加,这继发于肾小球血管阻力的显著降低。肾去神经支配可能会增强内源性血管紧张素II的活性,在这种情况下血管紧张素II会降低LpA,并可能调节急性肾去神经支配后肾血管阻力的最终水平。