Role of K‐Channels in Microvascular Flow‐ Induced Dilation of Subcutaneous and Visceral Arterioles in Human Obesity

Abstract

Altered vascular tone, a characteristic of human obesity, has been associated with impaired endothelium‐dependent vasodilation. Prior data suggest that visceral adipose tissue (VAT) is associated to endothelial dysfunction compared to subcutaneous adipose tissue (SAT). The aim of this study was to determine the contribution of vascular potassium channels to flow‐induced dilation (FID) in human VAT and SAT resistance arteries. Microvessels were obtained from VAT and SAT biopsies during bariatric surgery (OB; BMI>;48). Isolated vessels were cannulated for vascular reactivity to flow (pressure gradient 10–100 cmH2O) in the absence and presence of the 4‐aminopyridine (4‐AP; KV channel blocker), BaCl2 (KIR channel blocker), tetraethylammonium (TEA; BKCa channel blocker) and glybenclamide (KATP channel blocker). Dilations to papaverine (10–4M) were determined in each vessel. FID was reduced in VAT compared to SAT (at 60 cmH2O, 56±6% vs. 71±8%, p<0.05). There was no effect of TEA or glybenclamide on FID in SAT of OB subjects, but 4‐AP (p<0.05) and BaCl2 reduced FID in SAT of OB ( at 60 cmH2O and 100 cmH2O; p<0.05) vs. baseline. These data suggest that 1) FID is reduced in visceral compared to subcutaneous fat of obese patients and 2) Kir and Kv channels may be dysfunctional in VAT arterioles of obese subjects since 4‐AP and BaCl2 don't affect vasodilation of them while still reduce it in SAT arterioles.