Distinct cellular mechanisms of cholinergic and beta-adrenergic sweat secretion.
Am J Physiol
; 271(2 Pt 1): C486-94, 1996 Aug.
Article
in En
| MEDLINE
| ID: mdl-8769987
ABSTRACT
The cholinergic and beta-adrenergic sweat secretions from human sweat glands differ with respect to secretory rates and their susceptibility to cystic fibrosis (CF). Using the cultured beta-adrenergic-sensitive sweat secretory cell, we sought to determine the intracellular electrophysiological mechanisms underlying these functional differences. We found that the cholinergic agonist methacholine (10(-6) M) induced a Ca(2+)-dependent biphasic membrane potential (Vm) response an initial hyperpolarization and a secondary depolarization. The initial hyperpolarization was independent of bath Cl- and dependent on transmembrane K+ gradient. However, the secondary depolarization of Vm was dependent on bath Cl-. In contrast, the beta-adrenergic agonist isoproterenol (10(-5) M) induced a monophasic depolarization of Vm. This depolarization was 1) dependent on bath Cl-, 2) independent of K+ conductance (GK) blocker Ba2+ (5mM), 3) unaffected by the methacholine-induced secondary depolarization of Vm, and 4) absent in cells derived from CF subjects. These results indicated that the cholinergic agonist-induced secretion mainly involves the activation of Ca(2+)-dependent GK and Cl- conductance (GCl), whereas the beta-adrenergic secretion seems to mainly depend on the activation of cystic fibrosis transmembrane conductance regulator-GCl.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Skin
/
Sweat
/
Methacholine Chloride
/
Adrenergic beta-Agonists
/
Cholinergic Agents
/
Isoproterenol
Limits:
Humans
Language:
En
Journal:
Am J Physiol
Year:
1996
Document type:
Article
Affiliation country:
Estados Unidos