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Am J Physiol Heart Circ Physiol 275: H1449-H1454, 1998;
0363-6135/98 $5.00
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Vol. 275, Issue 4, H1449-H1454, October 1998

Role of K+ channels in arteriolar vasodilation mediated by integrin interaction with RGD-containing peptide

Steven H. Platts, Jon E. Mogford, Michael J. Davis, and Gerald A. Meininger

Microcirculation Research Institute, Department of Medical Physiology, Texas A & M University Health Science Center, College Station, Texas 77843-1114

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 alpha vbeta 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, Ca2+-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.

vascular smooth muscle; arteriole; microcirculation; cell signaling; arginine-glycine-asparagine


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