ABSTRACT
K + has been proposed to be E D H F in small arteries. Acetylcholine-stimulated, E D H F - mediated dilatation/relaxation was compared with raised [ K + ] 0 in rat mesenteric arteries. In pressurised arteries, acetylcholine (10~5 M ) dilated all arteries. Raising [K+] 0 from 5.88 to 10.58 m M only dilated a third of arteries tested. B a 2 + (3 x 10~ 5 M) did not affect dilatation to acetylcholine, but abolished those dilatations to raised [ K + ] G in some but not all arteries tested. In arteries suspended for isometric recording of force, acetylcholine (10~ 6 M) relaxed endothelium intact arteries, but not arteries without endothelium. Raising [ K + ] G from 5.9 to 10.9 m M failed to relax arteries in most cases. Under both isometric and pressurised conditions, relaxation and dilatation to raised [ K + ] Q was observed in the presence but not the absence of 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB), in preparations previously shown to be refractory to raised [ K + ] G . The effect was reversible, concentration-and endothelium-dependent. Under both pressurised and isometric conditions, the relaxation to elevated [ K + ] 0 in the presence of N P P B was completely reversed by B a 2 + (3 x 10~5 M ) . In presence of elevated [ K + ] 0 , N P P B and B a 2 + , acetycholine (10 uM) fully relaxed all arteries. Under isometric conditions, relaxations to elevated [ K + ] G could be revealed by hyperosmotic (plus 60 m M sucrose) superfusion. This effect was endothelium-dependent and was reversed by B a 2 + (3 x 10~5 M ) .
