Endothelium-dependent rhythmic contractions induced by cyclopiazonic acid, a sarcoplasmic reticulum Ca2+-pump inhibitor, in the rabbit femoral artery
| Autor: | Masayuki Omote, Hideo Mizusawa |
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| Rok vydání: | 1995 |
| Předmět: |
Male
medicine.medical_specialty Indoles Potassium Channels Vascular smooth muscle Charybdotoxin Endothelium Physiology Calcium-Transporting ATPases Femoral artery In Vitro Techniques Nitric Oxide Nitric oxide chemistry.chemical_compound Nifedipine medicine.artery Internal medicine medicine Animals heterocyclic compounds Phenylephrine Anatomy Femoral Artery Sarcoplasmic Reticulum medicine.anatomical_structure Endocrinology chemistry cardiovascular system Calcium Channels Endothelium Vascular Rabbits Cyclopiazonic acid medicine.drug |
| Zdroj: | Acta Physiologica Scandinavica. 154:113-119 |
| ISSN: | 1365-201X 0001-6772 |
| DOI: | 10.1111/j.1748-1716.1995.tb09893.x |
| Popis: | The vascular responses to cyclopiazonic acid (CPA), an inhibitor of the Ca(2+)-ATPase in the sarcoplasmic reticulum, were investigated in the rabbit femoral artery, suspended in an organ chamber for isometric tension recordings. CPA produced rhythmic contractions in the femoral artery which had been contracted with phenylephrine. CPA, however, did not induce the rhythmic responses in endothelium-denuded arteries. NG-nitro-L-arginine methyl ester and methylene blue, inhibitors of the formation and the action of nitric oxide, respectively, failed to antagonize the CPA-induced rhythmic contractions in the phenylephrine-contracted artery. In contrast, the CPA-induced rhythmic contractions were abolished by charybdotoxin, a Ca(2+)-activated K+ channel antagonist, but not by glibenclamide, a blocker of the ATP-sensitive K+ channel. Nifedipine also inhibited the CPA-induced rhythmic contractions in the endothelium-intact artery and relaxed the endothelium-denuded artery treated with CPA. These results indicate that the CPA-induced rhythmic contractions in the phenylephrine-contracted rabbit femoral artery may be attributed to the periodic inactivation of the voltage-dependent Ca2+ channel, presumably regulated by the Ca(2+)-activated K+ channel. The activation of the K+ channel by CPA might occur only when the endothelium is present. |
| Databáze: | OpenAIRE |
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