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Nitric oxide suppresses cerebral vasomotion by sGC-independent effects on ryanodine receptors and voltage-gated calcium channels


Reference:

Yuill, K. H., McNeish, A. J., Kansui, Y., Garland, C. J. and Dora, K. A., 2010. Nitric oxide suppresses cerebral vasomotion by sGC-independent effects on ryanodine receptors and voltage-gated calcium channels. Journal of Vascular Research, 47 (2), pp. 93-107.

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Official URL:

http://dx.doi.org/10.1159/000235964

Abstract

Background/Aims: In cerebral arteries, nitric oxide (NO) release plays a key role in suppressing vasomotion. Our aim was to establish the pathways affected by NO in rat middle cerebral arteries. Methods: In isolated segments of artery, isometric tension and simultaneous measurements of either smooth muscle membrane potential or intracellular [Ca2+] ([Ca2+](SMC)) changes were recorded. Results: In the absence of L -NAME, asynchronous propagating Ca2+ waves were recorded that were sensitive to block with ryanodine, but not nifedipine. L -NAME stimulated pronounced vasomotion and synchronous Ca2+ oscillations with close temporal coupling between membrane potential, tone and [Ca2+](SMC). If nifedipine was applied together with L -NAME, [Ca2+] C-SM decreased and synchronous Ca2+ oscillations were lost, but asynchronous propagating Ca2+ waves persisted. Vasomotion was similarly evoked by either iberiotoxin, or by ryanodine, and to a lesser extent by ODQ. Exogenous application of NONOate stimulated endothelium-independent hyperpolarization and relaxation of either L -NAME-induced or spontaneous arterial tone. NO-evoked hyperpolarization involved activation of BKCa channels via ryanodine receptors (RYRs), with little involvement of sGC. Further, in whole cell mode, NO inhibited current through L-type voltage-gated Ca2+ channels (VGCC), which was independent of both voltage and sGC. Conclusion: NO exerts sGC-independent actions at RYRs and at VGCC, both of which normally suppress cerebral artery myogenic tone. Copyright (C) 2009 S. Karger AG, Basel

Details

Item Type Articles
CreatorsYuill, K. H., McNeish, A. J., Kansui, Y., Garland, C. J. and Dora, K. A.
DOI10.1159/000235964
DepartmentsFaculty of Science > Pharmacy & Pharmacology
RefereedYes
StatusPublished
ID Code18119

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