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cGMP-dependent protein kinase activates Ca-activated K channels in cerebral artery smooth muscle cells.
TLDR
It is demonstrated that NO and a membrane-permeable analogue of cGMP can activate KCa channels in on-cell patches approximately twofold and cG MP-PK, in the presence of ATP andcGMP added directly to the intracellular surface of inside-out patches, increases channel activity by approximately eightfold. Expand
Evidence for a Functional Role of Endothelial Transient Receptor Potential V4 in Shear Stress–Induced Vasodilatation
TLDR
Ca2+ entry through endothelial TRPV4 channels triggers NO- and EDHF-dependent vasodilatation and appears to be mechanistically important in endothelial mechanosensing of shear stress. Expand
Systemic peripheral artery relaxation by KCNQ channel openers and hydrogen sulfide
TLDR
It is suggested that KCNQ channel opening is a powerful mechanism to produce vasorelaxation of systemic arteries in rats and mice and play a major role in the paracrine control of vascular tone by perivascular adipose tissue, which is at least in part mediated or modulated by H2S. Expand
Protein kinases: tuners of the BKCa channel in smooth muscle.
TLDR
The role ofprotein kinases in the regulation of BK(Ca) channels is discussed and many key issues, including the sites and mechanisms of actions of protein kinases, remain unresolved. Expand
The myogenic response: established facts and attractive hypotheses.
TLDR
While the primary mechanisms of the myogenic response are well understood, the details of the signalling pathways are still undefined and it is suggested that the clinical significance of theMyogenic response remains to be determined. Expand
The emerging role of Ca2+ sensitivity regulation in promoting myogenic vasoconstriction.
TLDR
The regulation of Ca2+ sensitivity, as an equal and complimentary partner ofCa2+-dependent processes, significantly enhances the authors' understanding of the complex array of signalling pathways, which ultimately mediate the myogenic response. Expand
Impaired Endothelium-Derived Hyperpolarizing Factor–Mediated Dilations and Increased Blood Pressure in Mice Deficient of the Intermediate-Conductance Ca2+-Activated K+ Channel
TLDR
The results indicate that the endothelial KCa3.1 is a fundamental determinant of endothelial hyperpolarization and EDHF signaling and, thereby, a crucial determinant in the control of vascular tone and overall circulatory regulation. Expand
Elevated Blood Pressure Linked to Primary Hyperaldosteronism and Impaired Vasodilation in BK Channel–Deficient Mice
TLDR
It is reported that deletion of the pore-forming BK channel &agr; subunit leads to a significant blood pressure elevation resulting from hyperaldosteronism accompanied by decreased serum K+ levels as well as increased vascular tone in small arteries. Expand
Mechanisms of NO/cGMP-dependent vasorelaxation.
TLDR
It is suggested that low physiological concentrations of NO decrease vascular tone through activation of cGKI, whereas high concentrations of DEA-NO relax vascular smooth muscle independent of c GKI and BK(Ca), which can relax small and large vessels by cGMP-dependentactivation of cAK. Expand
Iloprost activates KCa channels of vascular smooth muscle cells: role of cAMP-dependent protein kinase.
TLDR
The results show that iloprost is able to activate KCa channels of freshly isolated rat tail artery smooth muscle cells and suggest that this effect is mediated by a PKA-induced phosphorylation of the channel. Expand
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