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pubmed-article:2544103pubmed:dateCreated1989-7-18lld:pubmed
pubmed-article:2544103pubmed:abstractTextPrevious reports have suggested that organic calcium antagonists only partially inhibit the renal hemodynamic actions of angiotensin II (ANG II). This study tested the hypothesis that the calcium antagonist-sensitive component of ANG II-induced vasoconstriction is localized at a preglomerular site. Videomicroscopic measurements of vascular dimension were performed on in vitro blood-perfused juxtamedullary nephrons from captopril-treated rats. Under control conditions, afferent and efferent arteriolar diameters averaged 23.0 +/- 1.6 and 21.2 +/- 2.2 microns, respectively. Topical application of 0.1 nM ANG II decreased the diameters of afferent (-17 +/- 2%) and efferent (-15 +/- 3%) arterioles. Both 50 microM verapamil and 10 microM diltiazem dilated afferent arterioles. Verapamil also elicited a modest efferent vasodilation. In the presence of either verapamil or diltiazem, the effect of ANG II to decrease efferent diameter was sustained (-15 +/- 4%); however, the effect of ANG II on afferent diameter was abolished (-1 +/- 1%). These observations document differential influences of calcium channel blockers on ANG II-mediated vasoconstriction and suggest that the pre- and postglomerular vasoconstrictor actions of ANG II may occur through different calcium entry or mobilization mechanisms.lld:pubmed
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pubmed-article:2544103pubmed:authorpubmed-author:NavarL GLGlld:pubmed
pubmed-article:2544103pubmed:authorpubmed-author:CarminesP KPKlld:pubmed
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pubmed-article:2544103pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:2544103pubmed:articleTitleDisparate effects of Ca channel blockade on afferent and efferent arteriolar responses to ANG II.lld:pubmed
pubmed-article:2544103pubmed:affiliationDepartment of Physiology and Biophysics, University of Alabama, Birmingham 35294.lld:pubmed
pubmed-article:2544103pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:2544103pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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