Figure 2.

Cyclopiazonic acid-induced endothelium-dependent and extracellular K⁺-sensitive vasorelaxation of mesenteric arteries. (A) Representative tracings showing CPA or carbachol (CCh, 100 μM) induced endothelium-dependent vasorelaxation with intact endothelium (EC+, the left panel; the right panel) and the loss of vasorelaxation in response to CCh (100 μM) or CPA in endothelium-denuded arteries (EC−, the middle panel). (B) Summary data showing concentration-response curve (CRC), R_max, and EC₅₀ of CPA-induced vasorelaxation with intact endothelium (EC+, n = 6) or denuded endothelium (EC−, n = 6). (C) Representative tracings of CPA-induced concentration-dependent vasorelaxation in mesenteric arteries preconstricted with noradrenalin (5 μM NE, the left panel), and CPA or SNP concentration-dependent vasorelaxation in mesenteric arteries preconstricted with high extracellular K⁺ (80 mM KCl, the middle and the right panels). (D) Summary data showing the CRC, R_max, and EC₅₀ of CPA-induced vasorelaxation in mesenteric arteries preconstricted with norepinephrine (NE; n = 6) or KCl (n = 6). Data were expressed as percentage of NE‐ or KCl-induced vasoconstriction and shown as means ± SEM. ^**p < 0.01, ^***p < 0.001, ^****p < 0.0001.