Modulation of Ca2+ channels by opioid receptor antagonists in mesenteric arterial smooth muscle cells of rats in hemorrhagic shock.
The effects of hemorrhagic shock on Ba currents ( ) via Ca channels and the regulation of the channels in the vascular hyporesponse stage of hemorrhagic shock by opioid receptor antagonists were examined by using the whole-cell recording of patch-clamp technique in mesenteric arterial smooth muscle cells of rats. The results showed that hemorrhagic shock induced an inhibition of Ca channels in the cells; 10 micro M of naloxone and 100 n of naltrindole, nor-binaltorphimine, and beta-funaltrexamine increased the in the cells of rats in shock. After inhibition of protein kinase C by using 1-(5-isoquindinesulfonyl)-2-methylpiperazine via electrodes, the enhancement of by the antagonists was not observed. These results suggested that the inhibition of Ca channel induced by hemorrhagic shock was mediated by delta-, kappa-, and mu -opioid receptors in the cells and may be partly responsible for vascular hyporesponse. The enhancement of was mediated by activation of protein kinase C and may be responsible for the antagonist-caused improvement in the response of resistance arteries to vasoactive stimulants at the decompensatory stage of hemorrhagic shock.
D000818:Animals; D015220:Calcium Channels / Q000378:metabolism*; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D008638:Mesenteric Arteries / Q000187:drug effects* / Q000378:metabolism; D032389:Myocytes, Smooth Muscle / Q000187:drug effects* / Q000378:metabolism; D009292:Narcotic Antagonists / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D011957:Receptors, Opioid / Q000378:metabolism; D012771:Shock, Hemorrhagic / Q000378:metabolism*
D015220:Calcium Channels; D009292:Narcotic Antagonists; D011957:Receptors, Opioid