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Smooth muscle hyperpolarization originating in the endothelium and commonly referred to as the EDHF (endothelium-derived hyperpolarizing factor) response provides a very significant drive to vasodilatation particularly in small resistance arteries. Together with other endothelium-dependent dilator pathways 'EDHF' hyperpolarization is compromised by cardiovascular disease, including hypertension. However, although attenuated vascular hyperpolarization has been described in animal models of hypertension, the underlying mechanisms are not fully understood. In the current issue of the British Journal of Pharmacology, Weston et al. combine classic pharmacological approaches with electrophysiological and molecular techniques to suggest that attenuated endothelium-dependent hyperpolarization (and as a consequence vasodilatation) reflects major disruption of pathways associated with the activation of endothelial small conductance Ca(2+)-activated K-channels (SK(Ca)) in mesenteric arteries from spontaneously hypertensive rats. In addition to reductions in SK(Ca) and K(IR) proteins, changes in caveolin-1 isomers were also detected, possibly indicating channel realignment within plasmalemmal structures.

Original publication

DOI

10.1111/j.1476-5381.2010.00692.x

Type

Journal article

Journal

Br J Pharmacol

Publication Date

06/2010

Volume

160

Pages

833 - 835

Keywords

Animals, Antihypertensive Agents, Biological Factors, Down-Regulation, Hypertension, Membrane Microdomains, Membrane Potentials, Membrane Transport Modulators, Mesenteric Arteries, Potassium Channels, Inwardly Rectifying, Rats, Rats, Inbred SHR, Signal Transduction, Small-Conductance Calcium-Activated Potassium Channels, Vasodilation