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The obligatory link: role of gap junctional communication in endothelium-dependent smooth muscle hyperpolarization

Griffith, Tudor M., Chaytor, Andrew T. and Edwards, David Hughes 2004. The obligatory link: role of gap junctional communication in endothelium-dependent smooth muscle hyperpolarization. Pharmacological Research 49 (6) , pp. 551-564. 10.1016/j.phrs.2003.11.014

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Although an endothelium-derived hyperpolarizing factor (EDHF) has often been hypothesized to underpin vascular relaxations that are independent of nitric oxide (NO) and prostanoids, bioassay techniques have failed to confirm the existence of a freely transferable EDHF in a consistent fashion. Indeed, observations that inhibitors of direct cell–cell coupling such as connexin–mimetic peptides (e.g. Gap 26 and 27) and glycyrrhetinic acid derivatives attenuate “EDHF-type” smooth muscle hyperpolarizations and relaxations suggest that an electrotonic spread of endothelial hyperpolarization via myoendothelial and homocellular smooth muscle gap junctions plays an obligatory role in such responses. The endothelial hyperpolarization that initiates relaxation results from the opening of KCa channels and is sustained by capacitative Ca2+ entry triggered by the depletion of intracellular Ca2+ stores in the endoplasmic reticulum. EDHF-type relaxations are also associated with a prostanoid-independent synthesis of cAMP that increases the conductance of gap junction channels and enhances the transmission of endothelial hyperpolarization through the vascular wall in a permissive fashion. This review will discuss the roles of these interacting signalling pathways in the mediation of the EDHF phenomenon.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Subjects: R Medicine > R Medicine (General)
Publisher: Elsevier
ISSN: 1043-6618
Last Modified: 04 Jun 2017 08:03

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