Abstract:
NEW FINDINGS:What is the central question of this study? Calcium is an important second messenger in eccrine sweating; however, whether modulation of extracellular Ca(2+) and Ca(2+) entry has the capacity to modulate sweat rate in non-glabrous human skin has not been explored. What is the main finding and its importance? Acetylcholine to sweat rate dose-response relationships identify that local in vivo Ca(2+) chelation and L-type Ca(2+) channel antagonism have the capacity to attenuate the cholinergic sensitivity of eccrine sweat glands. Importantly, these data translate previous glabrous in vitro animal studies into non-glabrous in vivo human skin. Calcium is an important second messenger in eccrine sweating, with both internal and external sources being identified in vitro. It is unclear whether in vivo modulation of extracellular Ca(2+) levels or influx has the capacity to modulate sweat rate in non-glabrous human skin. To test the hypothesis that lowering interstitial Ca(2+) levels would decrease the sensitivity of the ACh to sweat rate (via capacitance hygrometry) dose-response relationship, nine healthy subjects received six ACh doses (1 × 10(-5) to 1 × 10(0) m in 10-fold increments) with and without a Ca(2+) chelator (12.5 mg ml(-1) EDTA) via forearm intradermal microdialysis (protocol 1). To test the hypothesis that attenuating Ca(2+) influx via L-type Ca(2+) channels would also decrease the sensitivity of the ACh to sweat rate dose-response relationship, 10 healthy subjects received similar ACh doses with and without a phenylalkylamine Ca(2+) channel blocker (1 mm verapamil; protocol 2). Non-linear regression curve fitting identified a right-shifted ED50 in EDTA-treated sites compared with ACh alone (-1.0 ± 0.1 and -1.5 ± 0.1 logm, respectively; P < 0.05), but unchanged maximal sweat rate (0.60 ± 0.07 and 0.58 ± 0.11 mg cm(-2) min(-1), respectively; P > 0.05) in protocol 1. Protocol 2 also resulted in a right-shifted ED(50) (verapamil, -0.9 ± 0.1 logm; ACh alone, -1.6 ± 0.2 logm; P < 0.05), with unchanged maximal sweat rate (verapamil, 0.45 ± 0.08 mg cm(-2) min(-1); ACh alone, 0.35 ± 0.06 mg cm(-2) min(-1); P > 0.05). Thus, local in vivo Ca(2+) chelation and L-type Ca(2+) channel antagonism have the capacity to attenuate in vivo cholinergic sensitivity of eccrine sweat glands. These data suggest that interstitial Ca(2+) and its influx via Ca(2+) channels play a functional role in eccrine sweating in intact non-glabrous human skin.
journal_name
Exp Physioljournal_title
Experimental physiologyauthors
Metzler-Wilson K,Sammons DL,Ossim MA,Metzger NR,Jurovcik AJ,Krause BA,Wilson TEdoi
10.1113/expphysiol.2013.076547subject
Has Abstractpub_date
2014-02-01 00:00:00pages
393-402issue
2eissn
0958-0670issn
1469-445Xpii
expphysiol.2013.076547journal_volume
99pub_type
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