CUTANEOUS ACTIVE VASODILATION IN HUMANS IS MEDIATED BY CHOLINERGIC NERVE COTRANSMISSION

During heat stress, increases in blood flow in nonglabrous skin in hum ans are mediated through active vasodilation by an unknown neurotransm itter mechanism. To investigate this mechanism, a three-part study was performed to determine the following: (1) Is muscarinic receptor acti vation necessary for active cutaneous vasodilation? We iontophoretical ly applied atropine to a small area of forearm skin. At that site and an untreated control site, we measured the vasomotor (laser-Doppler bl ood flow [LDF]) and sudomotor (relative humidity) responses to whole-b ody heat stress. Blood pressure was monitored. Cutaneous vascular cond uctance (CVC) was calculated (LDF divided by mean arterial pressure). Sweating was blocked at treated sites only. CVC rose at both sites (P< .05 at each site); thus, cutaneous active vasodilation is not effected through muscarinic receptors. (2) Are nonmuscarinic cholinergic recep tors present on cutaneous arterioles? Acetylcholine (ACh) was iontopho retically applied to forearm skin at sites pretreated by atropine iont ophoresis and at untreated sites. ACh increased CVC at untreated sites (P<.05) but not at atropinized sites. Thus, the only functional choli nergic receptors on cutaneous vessels art: muscarinic. (3) Does cutane ous active vasodilation involve cholinergic nerve cotransmission? Botu linum toxin was injected intradermally in the forearm to block release of ACh and any coreleased neurotransmitters. Heat stress was performe d as in part I of the study. At treated sites, CVC and relative humidi ty remained at baseline levels during heat stress (P>.05). Active vaso dilator and sudomotor responses to heat stress were abolished by botul inum toxin. We conclude that cholinergic nerve activation mediates cut aneous active vasodilation through release of an unknown cotransmitter , not through ACh.