FASEB J. Pierce now sold as Thermo Scientific
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Vivaudou, M. B.
Right arrow Articles by Singer, J. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Vivaudou, M. B.
Right arrow Articles by Singer, J. J.

The FASEB Journal, Vol 2, 2497-2504, Copyright © 1988 by The Federation of American Societies for Experimental Biology


RESEARCH COMMUNICATIONS

Regulation of one type of Ca2+ current in smooth muscle cells by diacylglycerol and acetylcholine

MB Vivaudou, LH Clapp, JV Walsh Jr and JJ Singer
Department of Physiology, University of Massachusetts Medical School, Worcester 01655.

Electrophysiological recordings from freshly dissociated smooth muscle cells from the stomach of the toad Bufo marinus revealed two types of Ca2+ currents. One has a low threshold of activation and inactivates rapidly; the other has a high threshold of activation and inactivates more slowly. Acetylcholine (ACh) increased the high-threshold current but not the low-threshold current. The synthetic diacylglycerol analog sn-1,2-dioctanoylglycerol, an activator of protein kinase C (PKC), mimicked these effects of ACh on Ca2+ currents. However, another diacylglycerol analog, 1,2-dioctanoyl-3-thioglycerol, which has a closely related structure but does not activate PKC, failed to increase the Ca2+ current. The same was true of 1,2-dioctanoyl-3- chloropropanediol, an analog that even at high concentrations only minimally activates PKC. These results suggest that diacylglycerol may be the second messenger mediating the effects of ACh on one type of voltage-activated Ca2+ channel, possibly by activating PKC.


This article has been cited by other articles:


Home page
J. Pharmacol. Exp. Ther.Home page
S. Bova, L. Trevisi, L. Cima, S. Luciani, V. Golovina, and G. Cargnelli
Signaling Mechanisms for the Selective Vasoconstrictor Effect of Norbormide on the Rat Small Arteries
J. Pharmacol. Exp. Ther., April 13, 2001; 296(2): 458 - 463.
[Abstract] [Full Text]


Home page
Physiol. Rev.Home page
M. J. Davis and M. A. Hill
Signaling Mechanisms Underlying the Vascular Myogenic Response
Physiol Rev, April 1, 1999; 79(2): 387 - 423.
[Abstract] [Full Text] [PDF]


Home page
Physiol. Rev.Home page
H. KURIYAMA, K. KITAMURA, T. ITOH, and R. INOUE
Physiological Features of Visceral Smooth Muscle Cells, With Special Reference to Receptors and Ion Channels
Physiol Rev, July 1, 1998; 78(3): 811 - 920.
[Abstract] [Full Text] [PDF]


Home page
J CARDIOVASC PHARMACOL THERHome page
W. H. Frishman
Mibefradil: A New Selective T-Channel Calcium Antagonist for Hypertension and Angina Pectoris
Journal of Cardiovascular Pharmacology and Therapeutics, January 1, 1997; 2(4): 321 - 330.
[Abstract] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1988 by The Federation of American Societies for Experimental Biology.