Cutaneous active vasodilation in XXXX is mediated by cholinergic nerve cotransmission.

@entity1 @entity455 @entity1617 @entity3897 @entity934
During heat stress, increases in blood flow in nonglabrous skin in @entity1 are mediated through active vasodilation by an unknown neurotransmitter mechanism. To investigate this mechanism, a three-part study was performed to determine the following: (1) Is muscarinic receptor activation necessary for active cutaneous vasodilation? We iontophoretically applied @entity3897 to a small area of forearm skin. At that site and an untreated control site, we measured the vasomotor (laser-Doppler blood flow [LDF]) and sudomotor (relative humidity) responses to whole-body heat stress. Blood pressure was monitored. @entity455 ( @entity455 ) was calculated (LDF divided by mean arterial pressure). Sweating was blocked at treated sites only. @entity455 rose at both sites (P < .05 at each site); thus, cutaneous active vasodilation is not effected through muscarinic receptors. (2) Are nonmuscarinic cholinergic receptors present on cutaneous arterioles? @entity934 ( @entity1617 ) was iontophoretically applied to forearm skin at sites pretreated by @entity3897 iontophoresis and at untreated sites. @entity1617 increased @entity455 at untreated sites (P < .05) but not at atropinized sites. Thus, the only functional cholinergic receptors on cutaneous vessels are muscarinic. (3) Does cutaneous active vasodilation involve cholinergic nerve cotransmission? Botulinum toxin was injected intradermally in the forearm to block release of @entity1617 and any coreleased neurotransmitters. Heat stress was performed as in part 1 of the study. At treated sites, @entity455 and relative humidity remained at baseline levels during heat stress (P > .05). Active vasodilator and sudomotor responses to heat stress were abolished by botulinum toxin. We conclude that cholinergic nerve activation mediates cutaneous active vasodilation through release of an unknown cotransmitter, not through @entity1617 .
