Endothelium‐dependent and independent effects of isoquercitrin in rat mesenteric bed involve nitric oxide production and direct activation of ATP‐sensitive K+ channels

Abstract

The vascular effect of isoquercitrin (ISQ), a flavonoid with putative cardioprotective effects, was investigated in perfused mesenteric vascular bed removed from naïve Wistar rats (females, 3–4 months). The perfusion pressure (PP) was measured under continuous flux of physiological saline solution (PSS, 4 ml/min) containing phenylephrine (10 μM). In endothelium‐intact tissue, PP was reduced by ISQ around 13, 33 and 60% at doses of 0.1, 0.3 and 1 μmol, respectively. Chemical removal of endothelium by sodium deoxycholate, as well as L‐NAME, an inhibitor of nitric oxide (NO) synthase, and the K+ channel blockers tetraethylammonium or iberiotoxin, partially avoided (~40%) the effects of 1 μmol of ISQ. The ATP‐sensitive K+ channel blocker glibenclamide (GLB, 10 μM) vanished the effects of ISQ at 0.1 and 0.3 μmol, but was ineffective against 1 μmol. However, infusion of GLB + L‐NAME, or high K+ (40 mM) solution, fully prevented the effects of ISQ. These results suggest that, in addition to previously showed angiotensin‐converting enzyme inhibition, the vascular effects of ISQ includes direct opening of ATP‐sensitive K+ channels and increased production of NO in resistance arteries.Research support: DEGPP/UNIPAR and CNPq/Brazil.