Enhanced b-receptor-mediated vasorelaxation in hypoxic porcine coronary artery

نویسندگان

  • SATORU FUKUDA
  • TAKASHI TORIUMI
  • HUI XU
  • HIDENORI KINOSHITA
  • HIRONOBU NISHIMAKI
  • SEIICHIRO KOKUBUN
  • NAOSHI FUJIWARA
  • HIDEYOSHI FUJIHARA
  • KOKI SHIMOJI
  • Takashi Toriumi
  • Hui Xu
  • Hidenori Kinoshita
  • Hironobu Nishimaki
  • Seiichiro Kokubun
  • Naoshi Fujiwara
  • Hideyoshi Fujihara
چکیده

Fukuda, Satoru, Takashi Toriumi, Hui Xu, Hidenori Kinoshita, Hironobu Nishimaki, Seiichiro Kokubun, Naoshi Fujiwara, Hideyoshi Fujihara, and Koki Shimoji. Enhanced b-receptor-mediated vasorelaxation in hypoxic porcine coronary artery. Am. J. Physiol. 277 (Heart Circ. Physiol. 46): H1447–H1452, 1999.—To investigate the b-adrenoceptor-mediated responses in hypoxic coronary arteries, we studied the effect of isoproterenol (Iso) on isolated porcine coronary arteries contracted with endothelin-1 in media aerated with 0, 5, 7.5, and 95% O2. The concentrationresponse curve of Iso was significantly shifted to the left by hypoxia (0 and 5% O2). In oxygenated and hypoxic arteries, 3 3 1028, 1026, and 1025 M Iso significantly increased the contents of cAMP. However, there was no difference in the increases of cAMP content induced by 3 3 1028 M Iso between oxygenated and hypoxic arteries. The content of cAMP induced by high concentrations of Iso (1026 and 1025 M) was significantly larger in hypoxic than in oxygenated arteries. Furthermore, the potentiation by hypoxia of the Iso-induced vasorelaxation was inhibited by glibenclamide and depolarization by KCl, but not by removal of endothelium and indomethacin. The vasodilatory response to forskolin and dibutyryl cAMP was unaffected by hypoxia. We conclude that activation of the ATP-sensitive K1 channel may account for the potentiation of the response to Iso in hypoxic coronary arteries.

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تاریخ انتشار 1999