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• W2076989031 abstract "Endothelium-dependent hyperpolarization of vascular smooth muscle provides a major pathway for relaxation in resistance arteries. This can occur due to direct electrical coupling via myoendothelial gap junctions (MEGJs) and/or the release of factors (EDHF). Here we provide evidence for the existence of functional MEGJs in the same, defined branches of BALB/C mouse mesenteric arteries which show robust EDHF-mediated smooth muscle relaxation. Cyclopiazonic acid (CPA, 10 µ<i>M</i>) was used to stimulate EDHF in arteries mounted under isometric conditions and constricted with phenylephrine. Simultaneous measurement of smooth muscle membrane potential and tension demonstrated that CPA caused a hyperpolarization of around 10 mV, reversing the depolarization to phenylephrine by 94% and the associated constriction by 66%. The relaxation to CPA was endothelium dependent, associated with the opening of Ca²⁺-activated K channels, and only in part due to the release of nitric oxide (NO). In the presence of the NO synthase inhibitor, <i>L</i>-NAME (100 µ<i>M</i>), the relaxation to CPA could be almost completely inhibited with the putative gap junction uncoupler, carbenoxolone (100 µ<i>M</i>). Inhibition of the synthesis of prostaglandins or metabolites of arachidonic acid had no effect under the same conditions, and small rises in exogenous K⁺ failed to evoke consistent or marked smooth muscle relaxation, arguing against a role for these molecules and ions as EDHF. Serial section electron microscopy revealed a high incidence of MEGJs, which was correlated with heterocellular dye coupling. Taken together, these functional and morphological data from a defined mouse resistance artery suggest that the EDHF response in this vessel may be explained by extensive heterocellular coupling through MEGJs, enabling spread of hyperpolarizing current." @default.
• W2076989031 created "2016-06-24" @default.
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• W2076989031 date "2003-01-01" @default.
• W2076989031 modified "2023-10-01" @default.
• W2076989031 title "Myoendothelial Gap Junctions May Provide the Pathway for EDHF in Mouse Mesenteric Artery" @default.
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• W2076989031 doi "https://doi.org/10.1159/000074549" @default.
• W2076989031 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/14583659" @default.
• W2076989031 hasPublicationYear "2003" @default.
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