Type 2 diabetes specifically attenuates purinergic skin vasodilatation without affecting muscarinic and nicotinic skin vasodilatation and sweating

Abstract

The present study evaluated whether type 2 diabetes (T2D) attenuates muscarinic and/or nicotinic cutaneous vasodilatation and sweating as well as purinergic cutaneous vasodilatation. Cutaneous vascular conductance and sweat rate were evaluated in 12 healthy nondiabetic older adults (Control, 60±8 years) and 13 older adults with T2D (62±10 years) at three intradermal forearm skin sites perfused with the following: 1) methacholine (muscarinic receptor agonist, 5 doses: 0.0125, 0.25, 5, 100, 2000 mM), 2) nicotine (nicotinic receptor agonist, 5 doses: 1.2, 3.6, 11, 33, 100 mM), or 3) ATP (purinergic receptor agonist, 5 doses: 0.03, 0.3, 3, 30, 300 mM). Each agonist was administered for 25 min per dose. At the end of the protocol, 50 mM sodium nitroprusside was administered to all skin sites to elicit maximum cutaneous vasodilatation. Cutaneous vascular conductance during methacholine and nicotine administration did not differ between groups (all P0.05). By contrast, cutaneous vascular conductance during administration of 30 mM (42±28 vs. 63±26 %max, P ≤ 0.05) and 300 mM ATP (56±24 vs. 71±20 %max, P ≤ 0.05) was attenuated in individuals with T2D in comparison to the Control participants. Further, cutaneous vascular conductance during administration of 50 mM sodium nitroprusside was lower in individuals with T2D relative to Control (P = 0.04). Methacholine- and nicotine-induced sweating was similar between groups (all P > 0.05). Thus, T2D attenuates purinergic mediated cutaneous vasodilatation without affecting muscarinic and nicotinic cutaneous vascular and sweating responses.