ISSN:
1432-2013
Keywords:
Glomerular filtration rate
;
Reninangiotensin system
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract In previous studies, we have shown that benzolamide, a carbonic anhydrase inhibitor with diuretic activity confined primarily to the proximal tubule, causes a significant reduction in nephron filtration rate by increasing afferent and efferent arteriolar vascular resistance [30], possibly through an activation of tubuloglomerular feedback mechanism. The present studies were designed to determine if infusion of 1-sar, 8-ala angiotensin II, an angiotensin II receptor antagonist (AIIA) could prevent and reverse the vasoconstriction and resulting reduction in SNGFR with benzolamide. Benzolamide administration to hydropenic rats decreased SNGFR by 5.0±1.3 nl/min and AIIA infusion in these rats completely restored SNGFR to the control, prebenzolamide values. These results occurred when SNGFR was measured in both proximal and distal tubules. In another group of hydropenic rats prior AIIA infusion completely prevented any alteration in SNGFR with benzolamide administration (33.0±2.8 vs. 32.3±1.5 nl/min). Benzolamide administration did increase the late proximal tubular flow rate during AIIA infusion (17.2±1.1 to 23.4±1.1 nl/min,P〈0.01), demonstrating that AIIA did not act by preventing the diuretic action of benzolamide in the proximal tubule. AIIA infusion alone did not alter control SNGFR or nephron plasma flow, suggesting that the effect of AIIA was not that of a non-specific vasodilator. These studies suggest that the renal vasoconstriction and reduction in SNGFR which results from benzolamide administration is mediated by the local action of angiotensin II.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00658483
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