Abstract

Isolated rabbit ear arteries displayed rhythmic contractions when stimulated with alpha 1 agonist phenylephrine. These rhythmic responses were greatly attenuated by endothelium removal. However, contractions were sufficiently rhythmic in the arteries treated with NG-monomethyl-L-arginine, NG-nitro-L-arginine and indomethacin, synthetic inhibitors of endothelium-derived nitric oxide and prostanoids. Phenylephrine-induced rhythmic contractions were converted to tonic contractions by the blockade both of the voltage-dependent Ca2+ channel and the Ca(2+)-activated K+ channel by nifedipine and charybdotoxin, respectively. In contrast, glibenclamide, an ATP-sensitive K+ channel antagonist, did not alter the rhythmic contractions. These results suggest that endothelium may in part regulate the phenylephrine-induced rhythmic contractions in the rabbit ear artery, although endothelium-derived nitric oxide or prostanoids may not be involved in these responses. These endothelium-involved rhythmic responses may be attributed to the activation of the voltage-dependent Ca2+ channel and the Ca(2+)-activated K+ channel.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.