Suppression of K +-induced hyperpolarization by phenylephrine in rat mesenteric artery: Relevance to studies of endothelium-derived hyperpolarizing factor

G. R. Richards, A. H. Weston, M. P. Burnham, M. Félétou, P. M. Vanhoutte, G. Edwards

    Research output: Contribution to journalArticlepeer-review

    Abstract

    In intact mesenteric arteries, increasing [K +] o by 5 mM hyperpolarized both endothelial and smooth muscle cells. Subsequent exposure to 10 μM phenylephrine depolarized both cell types which were then repolarized by a 5 mM increase in [K +] o. In endothelium-denuded vessels, increasing [K +] o by 5 mM hyperpolarized the smooth muscle but K + had no effect after depolarization by 10 μM phenylephrine. On subsequent exposure to iberiotoxin plus 4-aminopyridine, the repolarizing action of 5 mM K + was restored. In endothelium-intact vessels exposed to phenylephrine, pretreatment with a gap junction inhibitor (gap 27) reduced K +-mediated smooth muscle repolarization without affecting the endothelial cell response. It is concluded that phenylephrine-induced efflux of K + via smooth muscle K + channels produces a local increase in [K +] o which impairs repolarization to added K +. Thus, studies involving vessels precontracted with agonists which increase [K +] o maximize the role of gap junctions and minimize any contribution to the EDHF pathway from endothelium-derived K +.
    Original languageEnglish
    Pages (from-to)1-5
    Number of pages4
    JournalBritish Journal of Pharmacology
    Volume134
    Issue number1
    DOIs
    Publication statusPublished - 2001

    Keywords

    • EDHF
    • Endothelium
    • Hyperpolarization
    • K +
    • K + channels
    • Repolarizarion
    • Smooth muscle

    Fingerprint

    Dive into the research topics of 'Suppression of K +-induced hyperpolarization by phenylephrine in rat mesenteric artery: Relevance to studies of endothelium-derived hyperpolarizing factor'. Together they form a unique fingerprint.

    Cite this