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Am J Physiol Lung Cell Mol Physiol 262: L100-L104, 1992;
1040-0605/92 $5.00
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AJP - Lung Cellular and Molecular Physiology, Vol 262, Issue 1 100-L104, Copyright © 1992 by American Physiological Society


ARTICLES

Inositol 1,4,5-trisphosphate, inositide flux rates and pool sizes during smooth muscle relaxation

C. B. Baron, J. N. Pompeo and R. F. Coburn
Department of Physiology, University of Pennsylvania, Philadelphia 19104-6085.

Decreases in D-myo-inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] content and changes in inositol phospholipid contents occurred during the time of atropine-induced relaxation of swine tracheal smooth muscle contracted with 55 microM carbachol. Decrease in Ins(1,4,5)P3 occurred in a pool which makes up 40% of the total content of this inositol phosphate and which has access to Ins(1,4,5)P3 5-phosphatase and/or 3-kinase. A 50% decrease in this pool occurred at 16 s after addition of atropine and within 6-10 s after inhibition of phospholipase C (PLC). The maximal fall in Ins(1,4,5)P3 occurred at a time when force had only decreased 30% of the maximal response. A phosphatidylinositol 4-phosphate (PIP) pool linked to muscarinic receptor-activation increased 160% after addition of atropine, the maximal response occurring at a time when relaxation was 80% complete. The mechanisms for this increase were the maintained formation of PIP and phosphatidylinositol 4,5-bisphosphate (PIP2) even though PIP2 hydrolysis was inhibited and the apparent chemical equilibrium between PIP and PIP2.


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D. Sul, C. B. Baron, R. Broome, and R. F. Coburn
Smooth muscle length-dependent PI(4,5)P2 synthesis and paxillin tyrosine phosphorylation
Am J Physiol Cell Physiol, July 1, 2001; 281(1): C300 - C310.
[Abstract] [Full Text] [PDF]




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