Regulation of blood flow in adipose tissue: involvement of the cholinergic system

Abstract

Acetylcholine (Ach) has vasodilatory actions. However, data are conflicting about the role of Ach in regulating blood flow in subcutaneous adipose tissue (ATBF). This may be related to inaccurate ATBF recording or to the responder/nonresponder (R/NR) phenomenon. We showed previously that healthy individuals are R (ATBF increases postprandially by >50% of baseline BF) or NR (ATBF increases ≤50% postprandially). Our objective was to assess the role of the cholinergic system on ATBF in R and NR subjects. ATBF was manipulated by in situ microinfusion of vasoactive agents (VA) in AT and monitored by the 133Xenon washout technique (both recognized methods) at the VA site and at the control site. We tested incrementally increasing doses of Ach (10−5, 10−3, and 10−1 mol/l; n = 15) and Ach receptor antagonists (Ra) before and after oral administration of 75-g glucose using atropine (muscarinic Ra; 10−4 mol/l, n = 13; 10−5 mol/l, n = 22) and mecamylamine (nicotinic Ra; 10−3 mol/l, n = 15; 10−4 mol/l, n = 10). Compared with baseline [2.41 (1.36–2.83) ml·100 g−1·min−1], Ach increased ATBF dose dependently [3.32 (2.80–5.09), 6.46 (4.36–9.51), and 10.31 (7.98–11.52), P < 0.0001], with no difference between R and NR. Compared with control side, atropine (both concentrations) had no effect on fasting ATBF; only atropine 10−4 mol/l decreased post-glucose ATBF [iAUC: 1.25 (0.32–2.91) vs. 1.98 (0.64–2.94); P = 0.04]. This effect was further apparent in R. Mecamylamine had no impact on fasting and postglucose ATBF in R and NR. Our results suggest that the cholinergic system is implicated in ATBF regulation, although it has no role in the blunting of ATBF response in NR.