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Central role of heterocellular gap junctional communication in endothelium-dependent relaxations of rabbit arteries

Chaytor, A. T., Evans, William Howard and Griffith, T. H. 1998. Central role of heterocellular gap junctional communication in endothelium-dependent relaxations of rabbit arteries. The Journal of Physiology 508 (2) , pp. 561-573. 10.1111/j.1469-7793.1998.561bq.x

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Abstract

1. The contribution of gap junctions to endothelium-dependent relaxation was investigated in isolated rabbit conduit artery preparations pre-constricted by 10 μM phenylephrine (PhE).2Acetylcholine (ACh) relaxed the thoracic aorta by ≈60 % and the superior mesenteric artery (SMA) by ≈90 %. A peptide possessing sequence homology with extracellular loop 2. of connexin 43 (Gap 27, 300 μM) inhibited relaxation by ≈40 % in both artery types. Gap 27 also attenuated the endothelium-dependent component of the relaxation induced by ATP in thoracic aorta but did not modify force development in response to PhE. 3. NG-nitro-L-arginine methyl ester (L-NAME, 300 μM), an inhibitor of NO synthase, attenuated ACh-induced relaxation by ≈90 % in the aorta but only by ≈40 % in SMA (P < 0.05). Residual L-NAME-insensitive relaxations were almost abolished by 300 μM Gap 27 in aorta and inhibited in a concentration-dependent fashion in SMA (≈50 % at 100 μM and ≈80 % at 10 mM). Gap 27 similarly attenuated the endothelium-dependent component of L-NAME-insensitive relaxations to ATP in aorta. 4. Responses to cyclopiazonic acid, which stimulates endothelium-dependent relaxation through a receptor-independent mechanism, were also attenuated by Gap 27, whereas this peptide exerted no effect on the NO-mediated relaxation induced by sodium nitroprusside in preparations denuded of endothelium. 5. ACh-induced relaxation of ‘sandwich’ mounts of aorta or SMA were unaffected by Gap 27 but completely abolished by L-NAME. 6. We conclude that direct heterocellular communication between the endothelium and smooth muscle contributes to endothelium-dependent relaxations evoked by both receptor-dependent and -independent mechanisms. The inhibitory effects of Gap 27 peptide do not involve homocellular communication within the vessel wall or modulation of NO release or action.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Subjects: R Medicine > R Medicine (General)
Publisher: The Physiological Society
ISSN: 0022-3751
Last Modified: 17 Mar 2021 02:56
URI: https://orca.cardiff.ac.uk/id/eprint/66746

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