Acetylcholine-induced relaxation and hyperpolarization in small bovine adrenal cortical arteries: Role of cytochrome P450 metabolites
Endocrinology, ISSN: 0013-7227, Vol: 145, Issue: 10, Page: 4532-4539
2004
- 8Citations
- 8Captures
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Metrics Details
- Citations8
- Citation Indexes8
- CrossRef3
- Captures8
- Readers8
Article Description
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 to 10 M) elicited a concentration-dependent relaxation, with a maximal relaxation of 96 ± 1% and EC 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 μM) but not by the cyclooxygenase inhibitor indomethacin (10 μM). The maximal relaxation and EC 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 μM) and miconazole (10 μM). The maximal relaxations and ECs with SKF 525A and miconazole were 56 ± 8 and 72 ± 2% and 0.8 and 0.5 μM, 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 to 10 M) and 14,15-epoxyeicosatrienoic acid (14,15-EET, 10 to 10 M), a cytochrome P450 metabolite of arachidonic acid, also evoked relaxations in small adrenal arteries, with maximal relaxations of 56 ± 4 and 90 ± 5%, respectively. The arachidonic acid-induced relaxation was blocked by SKF 525A. Using high-pressure liquid chromatography and gas chromatography/mass spectrometry analysis, EETs were identified in small adrenal arteries. These results demonstrate that acetylcholine is a potent vasodilator of small adrenal cortical arteries. The acetylcholine-induced relaxation is largely mediated by an endothelium-dependent hyperpolarization mechanism, presumably through cytochrome P450 metabolites of arachidonic acid.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=4644284906&origin=inward; http://dx.doi.org/10.1210/en.2004-0450; http://www.ncbi.nlm.nih.gov/pubmed/15231705; https://academic.oup.com/endo/article-lookup/doi/10.1210/en.2004-0450; https://dx.doi.org/10.1210/en.2004-0450; https://academic.oup.com/endo/article-abstract/145/10/4532/2499765?redirectedFrom=fulltext
The Endocrine Society
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