Lack of direct effect of adiponectin on vascular smooth muscle cell BK(Ca) channels or Ca(2+) signaling in the regulation of small artery pressure‐induced constriction

The aim of this study was to investigate mechanisms by which adiponectin influences vascular Ca(2+) signaling, K(+) channel activity and thus contractile tone of small arteries. Vasodilation to adiponectin was studied in mesenteric resistance arteries constricted with intraluminal pressure. Ca(2+) signals were characterized using high speed confocal microscopy of intact arteries. Patch clamp investigated the effect of adiponectin on individual VSMC potassium (K(+)) channel currents. Adiponectin dilated arteries constricted with pressure‐induced tone by approximately 5% and the induced vasodilation was only transient. The dilation to adiponectin was reduced by pharmacological interruption of the Ca(2+) spark/large conductance activated K(+) (BK) channel pathway but from a physiological perspective, interpretation of the data was limited by the small effect. Neither Adiponectin nor the presence of intact perivascular adipose tissue (PVAT) influenced Ca(2+) spark or Ca(2+) wave frequency or characteristics. Studied using a perforated patch approach, Adiponectin marginally increased current through the VSMC BK channel but this effect was lost using the whole cell technique with dialysis of the cytoplasm. Adiponectin did not change the frequency or amplitude of Ca(2+) spark‐induced transient outward currents (STOC). Overall, our study shows that Adiponectin induces only a small and transient dilation of pressure constricted mesenteric arteries. This vasodilatory effect is likely to be independent of Ca(2+) sparks or direct BK channel activation.