Previous 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 dimensions 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 μm, respectively. Topical application of 0.1 nM ANG II decreased the diameters of afferent (-17 ± 2%) and efferent (-15 ± 3%) arterioles. Both 50 μM verapamil and 10 μM diltiazem dilated afferent arterioles. Verapamil also elicitied a modest efferent vasodilation. In the presence of either verapamil or diltiazem, the effects 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.
|Original language||English (US)|
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|Publication status||Published - Jan 1 1989|
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