Acetylcholine-induced relaxation and hyperpolarization in small bovine adrenal cortical arteries: role of cytochrome P450 metabolites

Endocrinology
David X ZhangW B Campbell

Abstract

The present study characterizes the vascular responses of isolated small bovine adrenal cortical arteries to acetylcholine, an endogenous neurotransmitter in the adrenal gland. Acetylcholine (10(-10) to 10(-6) m) elicited a concentration-dependent relaxation, with a maximal relaxation of 96 +/- 1% and EC50 of 4.2 nm. The relaxation was abolished by endothelial removal and attenuated by the nitric oxide synthase inhibitor N-nitro-L-arginine (L-NA, 30 microm) but not by the cyclooxygenase inhibitor indomethacin (10 microm). The maximal relaxation and EC50 of acetylcholine in the presence of L-NA were 87 +/- 4% and 22 nm, respectively. The acetylcholine-induced, indomethacin- and L-NA-resistant relaxation was eliminated by high K+ and markedly inhibited by the cytochrome P450 inhibitors SKF 525A (10 microm) and miconazole (10 microm). The maximal relaxations and EC50s with SKF 525A and miconazole were 56 +/- 8 and 72 +/- 2% and 0.8 and 0.5 microm, respectively. In indomethacin- and L-NA-treated arteries, acetylcholine induced a smooth muscle hyperpolarization, which was blocked by SKF 525A (3 +/- 1 mV vs. 15 +/- 2 mV of control). Arachidonic acid (10(-9) to 10(-5) m) and 14,15-epoxyeicosatrienoic acid (14,15-EET, 10(-9) to 10(-5) ...Continue Reading

Citations

Dec 3, 2008·Hypertension·Robert S Danziger
Oct 17, 2006·American Journal of Physiology. Heart and Circulatory Physiology·Nitin T AggarwalWilliam B Campbell
Apr 21, 2007·Endocrinology·David X ZhangWilliam B Campbell
May 14, 2005·Endocrinology·Kathryn M GauthierWilliam B Campbell
Aug 4, 2005·American Journal of Physiology. Endocrinology and Metabolism·David X ZhangWilliam B Campbell

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