Role of heterocellular gap junctional communication in endothelium-dependent smooth muscle hyperpolarization: Inhibition by a connexin-mimetic peptide

被引:108
作者
Dora, KA
Martin, PEM
Chaytor, AT
Evans, WH
Garland, CJ
Griffith, TM
机构
[1] Cardiff Univ, Cardiovasc Sci Res Grp, Dept Radiol, Cardiff CF4 4XN, S Glam, Wales
[2] Cardiff Univ, Cardiovasc Sci Res Grp, Dept Med Biochem, Cardiff CF4 4XN, S Glam, Wales
[3] Univ Bristol, Dept Pharmacol, Bristol BS8 1TD, Avon, England
基金
英国惠康基金;
关键词
gap junctions; endothelium-dependent hyperpolarization; acetylcholine; levcromakalim; Lucifer yellow;
D O I
10.1006/bbrc.1998.9877
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
A synthetic connexin-mimetic peptide (Gap 27 peptide) was used to evaluate the contribution of gap junctional communication to smooth muscle responses mediated by the endothelium-dependent agonist acetylcholine (ACh) in rabbit mesenteric arteries. Hyperpolarizations and relaxations to 0.1 and 1 mu M ACh observed in the presence of nitric oxide synthase and cyclooxygenase inhibition were markedly attenuated by the peptide at a concentration of 300 mu M, whereas the hyperpolarizing response to levcro-makalim, a K-ATP channel opener, was unaffected. The peptide also attenuated intercellular transfer of Lucifer yellow in confluent cultures of COS-7 cells, thus confirming its ability to modulate the permeability of gap junctions. The findings demonstrate that heterocellular gap junctional communication contributes to NO- and prostanoid-independent mechanisms of vasorelaxation that are widely attributed to an endothelium-derived hyperpolarizing factor. (C) 1999 Academic Press.
引用
收藏
页码:27 / 31
页数:5
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