Histamine-induced calcium release and phorbol antagonism in cultured airway smooth muscle cells

Histamine-induced calcium release and phorbol antagonism in cultured airway smooth muscle cells clinical and physiological importance. The mechanism of histamine activation of airway is of special importance, since altered sensitivity of this tissue to histamine is a fundamental feature of asthma (8). Despite this fact, little direct information about the action of histamine on airway cells exists. The degree to which contraction of airway is mediated by release of intracellular , in contrast to influx of through specific membrane channels, is unclear. Studies have demonstrated a marked dependence of histamine contraction on external concentration (14), a partial antagonism of contraction by channel antagonists (7, 11) or no detectable influx (1). Recent studies in whole tissue suggest that histamine receptor coupling results in inositol phospholipid breakdown in (10). Thus histamine activation of would be expected to involve inositol trisphosphate (IP3) -triggered release of from the THE EFFECTS OF HISTAMINE are of widespread sarcoplasmic reticulum (5,2l) and sn-1,2diacylglycerolstimulated activation of c kinase, a Ca2+ and phospholipid-sensitive enzyme with important physiological actions (15). However, since histamine affects neural and other cellular elements intimately associated with myocytes, the extent to which studies conducted in whole tissue preparations reflect the direct response of the cell to the agonist are unclear. The direct nature of the http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Cell Physiology The American Physiological Society

Histamine-induced calcium release and phorbol antagonism in cultured airway smooth muscle cells

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Publisher
The American Physiological Society
Copyright
Copyright © 1987 the American Physiological Society
ISSN
0363-6143
eISSN
1522-1563
Publisher site
See Article on Publisher Site

Abstract

clinical and physiological importance. The mechanism of histamine activation of airway is of special importance, since altered sensitivity of this tissue to histamine is a fundamental feature of asthma (8). Despite this fact, little direct information about the action of histamine on airway cells exists. The degree to which contraction of airway is mediated by release of intracellular , in contrast to influx of through specific membrane channels, is unclear. Studies have demonstrated a marked dependence of histamine contraction on external concentration (14), a partial antagonism of contraction by channel antagonists (7, 11) or no detectable influx (1). Recent studies in whole tissue suggest that histamine receptor coupling results in inositol phospholipid breakdown in (10). Thus histamine activation of would be expected to involve inositol trisphosphate (IP3) -triggered release of from the THE EFFECTS OF HISTAMINE are of widespread sarcoplasmic reticulum (5,2l) and sn-1,2diacylglycerolstimulated activation of c kinase, a Ca2+ and phospholipid-sensitive enzyme with important physiological actions (15). However, since histamine affects neural and other cellular elements intimately associated with myocytes, the extent to which studies conducted in whole tissue preparations reflect the direct response of the cell to the agonist are unclear. The direct nature of the

Journal

AJP - Cell PhysiologyThe American Physiological Society

Published: Oct 1, 1987

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