# MECHANISM OF ECCRINE SWEAT GLAND FUNCTION

> **NIH NIH R01** · UNIVERSITY OF IOWA · 1991 · $220,862

## Abstract

DESCRIPTION (Adapted from the applicant's abstract):  The eccrine sweat
gland, one of the major cutaneous appendages, serves primarily for
thermoregulation.  However, its importance in cutaneous pathophysiology has
not been fully understood.  The primary goal of the present proposal is to
clarify the basic mechanisms of eccrine sweating at the cellular and
membrane levels.  Eccrine sweat secretion is the consequence of a sequence
of events beginning with agonist-receptor interaction, followed by
receptor-mediated membrane events (e.g., activation of G-protein,
phosphatidylinositol metabolism, and calcium(Ca)-channels) and
intracellular events (e.g., activation of various kinases, the cytoskeletal
system, cAMP, Ca/C calmodulin systems, and intracellular pH), resulting
ultimately in activation of membrane transport (e.g., activation of
chloride (Cl) and potassium (K) channels, cotransporters, and parallel
transporters).  Previous studies indicate that activation of Cl and K
channels may be of crucial importance in the activation of membrane
transport during sweat secretion.  Further understanding of Cl channel
regulation will help solve the pathogenesis of cystic fibrosis (CF).  Since
the eccrine sweat gland is regulated by multiple neurotransmitters or
modulators (vasoactive intestinal peptides, ATP, prostaglandins,
interleukins, and cholinergic and adrenergic agonists), the regulatory role
of each of these agents must be clarified.  Innovative new methods for
studying the regulation of membrane transport, K and Cl channels, and
transporters in the sweat gland cells, namely, cell volume analysis and
patch clamp methods, will be used.  Interleukin 1 (IL-1) is abundantly
present in human eccrine sweat and its function must be addressed.  The
normal function of the mouse sweat gland must be known so as to compare it
with (especially CF) transgenic mice.  Diagnostic guidelines and
methodologies for disorders of eccrine sweating must be developed.

The specific aims of this proposal are as follows:  (1) To study the
regulation of ionic channels and transporters in freshly dissociated native
human and rhesus eccrine clear cell using cell volume analysis; (2) to
study further the regulation of K and Cl channels using patch clamp
techniques during cell volume regulation, pharmacological stimulation, and
intracellular application of various modulators, inhibitors, and antibodies
(against various cellular components); (3) to study the function of Il-1 on
ion channel activity, cytoplasmic pH, and Ca and to study regulation of
IL-1 synthesis using Northern blotting and quantitative PCR techniques; (4)
to study the pharmacology and function of the mouse eccrine sweat gland as
a prelude to studying cystic fibrosis transgenic mice, and (5) to develop
diagnostic methodologies and guidelines for clinical disorders of eccrine
sweating.

## Key facts

- **NIH application ID:** 3155296
- **Project number:** 2R01AR025339-14
- **Recipient organization:** UNIVERSITY OF IOWA
- **SAM.gov UEI:** Z1H9VJS8NG16
- **Principal Investigator:** KENZO SATO
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1991
- **Award amount:** $220,862
- **Award type:** 2
- **Project period:** 1978-06-01 → 1995-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3155296

## Citation

> US National Institutes of Health, RePORTER application 3155296, MECHANISM OF ECCRINE SWEAT GLAND FUNCTION (2R01AR025339-14). Retrieved via MORVS 2026-10-24 from https://api.morvs.ai/grant/nih/3155296. Licensed CC0.

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