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Submitted on February 1, 2005
Accepted on May 4, 2005
Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI 53226
* To whom correspondence should be addressed. E-mail: wbcamp{at}mcw.edu.
Adrenal steroidogenesis is modulated by humoral and neuronal factors and blood flow. Angiotensin II (AII) stimulates adrenal cortical aldosterone and cortisol production and medullary catecholamine release. However, AII regulation of adrenal vascular tone has not been characterized. We examined the effect of AII on diameters of cannulated bovine adrenal cortical arteries. Cortical arteries (average internal diameter = 230 µm) were constricted with U46619 and concentration-diameter responses to AII (10-13 to 10-8 mol/liter) were measured. In endothelium-intact arteries, AII induced dilations at low concentrations (maximum dilation = 25 ± 6% at 10-10 mol/liter) and constrictions at high concentrations (maximum constriction = 25 ± 18% at 10-8 mol/liter). AII constrictions were blocked by the angiotensin type 1 (AT1) receptor antagonist, losartan (10-6 mol/liter). AII dilations were enhanced by losartan (maximal dilation = 48 ± 8%), abolished by endothelial cell removal or N-nitro-L-arginine (L-NA, 3 x 10-5 mol/liter) and inhibited by the angiotensin type 2 (AT2) receptor antagonist, PD123319 (10-6 mol/liter, maximal dilation = 18 ± 4%). In a 4,5-diaminofluorescein diacetate nitric oxide (NO) assay of isolated cortical arteries, AII stimulated NO production which was abolished by PD123319, L-NA or endothelial cell removal. Western immunoblot of arterial homogenates and endothelial and zona glomerulaosa cell lysates revealed a 48 kD band and 50 kD band corresponding to AT1 and AT2 receptors, respectively, in all three and a 140 kD band corresponding to endothelial NO synthase in endothelial cells and arteries. Our results demonstrate that AII stimulates adrenal cortical arterial dilation through endothelial cell AT2 receptor activation and NO release and AT1 receptor-dependent constriction.
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