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Matches in SemOpenAlex for { <https://semopenalex.org/work/W2187320736> ?p ?o ?g. }

• W2187320736 endingPage "H1454" @default.
• W2187320736 startingPage "H1449" @default.
• W2187320736 abstract "Integrins are transmembrane adhesion receptors found on most cells, including vascular smooth muscle cells. Several integrins bind to the conserved amino acid sequence Arg-Gly-Asp (RGD), and synthetic RGD-containing peptides can cause endothelium-independent arteriolar vasodilation by interacting with the α v β 3 -integrin expressed by vascular smooth muscle. We hypothesized that RGD peptide-induced vasodilation involves K + channels. Rat cremaster arterioles were treated with cRGD (GPenGRGDSPCA) in the presence or absence of the nonselective K + channel inhibitor tetraethylammonium (TEA, 20 mM). TEA caused arterioles to constrict by 19 ± 5% and inhibited cRGD-induced vasodilation ( n = 7, P < 0.05). Vessels preconstricted with phenylephrine (5 × 10 −7 M) showed no significant inhibition of the dilatory response to cRGD, indicating that inhibition by TEA was not related to increased vasomotor tone. Further evidence for the involvement of K + channels was obtained by addition of 100 mM KCl ( n = 5), which inhibited vasodilation caused by cRGD. Inhibition of large and small conductance, Ca 2+ -activated K + channels with iberiotoxin (100 nM) or apamin (25 nM), respectively, had no effect on cRGD-induced vasodilation. Partial inhibition of vasodilation was observed with inhibitors of voltage-gated (4-aminopyridine, 1 mM), ATP-sensitive (glibenclamide, 1 μM), and inward rectifying (barium, 50 μM) K + channels. These data support the hypothesis that integrin-signaling pathways leading to arteriolar vasodilation may involve modulation of K + channel function." @default.
• W2187320736 created "2016-06-24" @default.
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• W2187320736 date "1998-10-01" @default.
• W2187320736 modified "2023-09-26" @default.
• W2187320736 title "Role of K⁺channels in arteriolar vasodilation mediated by integrin interaction with RGD-containing peptide" @default.
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• W2187320736 doi "https://doi.org/10.1152/ajpheart.1998.275.4.h1449" @default.
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