Gap junction-dependent and -independent EDHF-type relaxations may involve smooth muscle cAMP accumulation

DOI Web Site 被引用文献3件
  • Andrew T. Chaytor
    Department of Diagnostic Radiology, Wales Heart Research Institute, University of Wales College of Medicine, Cardiff CF14 4XN, United Kingdom
  • Hannah J. Taylor
    Department of Diagnostic Radiology, Wales Heart Research Institute, University of Wales College of Medicine, Cardiff CF14 4XN, United Kingdom
  • Tudor M. Griffith
    Department of Diagnostic Radiology, Wales Heart Research Institute, University of Wales College of Medicine, Cardiff CF14 4XN, United Kingdom

書誌事項

公開日
2002-04-01
DOI
  • 10.1152/ajpheart.00903.2001
公開者
American Physiological Society

この論文をさがす

説明

<jats:p> We have compared the mechanisms that contribute to endothelium-derived hyperpolarizing factor (EDHF)-type responses induced by ACh and the Ca<jats:sup>2+</jats:sup> ionophore A-23187 in the rabbit iliac artery. Relaxations to both agents were associated with ∼1.5-fold elevations in smooth muscle cAMP levels and were attenuated by the adenylyl cyclase inhibitor 2′,5′-dideoxyadenosine (DDA) and potentiated by the cAMP phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). Mechanical responses were inhibited by coadministration of the Ca<jats:sup>2+</jats:sup>-activated K<jats:sup>+</jats:sup>channel blockers apamin and charybdotoxin, both in the absence and presence of IBMX, but were unaffected by blockade of ATP-sensitive K<jats:sup>+</jats:sup> channels with the sulphonylurea glibenclamide. Relaxations and elevations in cAMP evoked by ACh were abolished by 18α-glycyrrhetinic acid, which disrupts gap junction plaques, whereas the corresponding responses to A-23187 were unaffected by this agent. Consistently, in “sandwich” bioassay experiments, A-23187, but not ACh, elicited extracellular release of a factor that evoked relaxations that were inhibited by DDA and potentiated by IBMX. These findings provide evidence that EDHF-type relaxations of rabbit iliac arteries evoked by ACh and A-23187 depend on cAMP accumulation in smooth muscle, but involve signaling via myoendothelial gap junctions and the extracellular space, respectively. </jats:p>

収録刊行物

被引用文献 (3)*注記

もっと見る

詳細情報 詳細情報について

問題の指摘

ページトップへ