Abstract
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) |
|---|---|
| Pages (from-to) | F1015-F1020 |
| Journal | American Journal of Physiology - Renal Fluid and Electrolyte Physiology |
| Volume | 256 |
| Issue number | 6 (25/6) |
| DOIs | |
| State | Published - 1989 |
| Externally published | Yes |
ASJC Scopus subject areas
- Physiology