JPET xPharm- The Comprehensive Pharmacology Reference

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rapoport, R. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rapoport, R. M.

Effects of norepinephrine on contraction and hydrolysis of phosphatidylinositols in rat aorta

RM Rapoport

The purpose of this study was to investigate the relationship between norepinephrine-induced contraction and hydrolysis of phosphatidylinositols in rat aorta. Norepinephrine-induced contraction was associated with increased accumulation of the hydrolytic products of the phosphatidylinositols, inositol monophosphate and phosphatidic acid. Norepinephrine also induced significant decreases in phosphatidylinositol phosphate and phosphatidylinositol bisphosphate. The alpha-1 adrenoceptor antagonist, prazosin, exposure to the Ca++ channel modulator, nifedipine, and removal of extracellular Ca++ inhibited the accumulation of inositol monophosphate and contraction due to norepinephrine. These results suggest that the contraction induced by norepinephrine may be mediated by processes associated with hydrolysis of phosphatidylinositols. The hydrolysis may occur through Ca++-dependent activation of phospholipase C by alpha-1 adrenoceptor agonists.

Volume 242, Issue 1, pp. 188-194, 07/01/1987
Copyright © 1987 by American Society for Pharmacology and Experimental Therapeutics




This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
M. Tosun, Y. Erac, C. Selli, and N. Karakaya
Sarcoplasmic-endoplasmic reticulum Ca2+-ATPase inhibition prevents endothelin A receptor antagonism in rat aorta
Am J Physiol Heart Circ Physiol, April 1, 2007; 292(4): H1961 - H1966.
[Abstract] [Full Text] [PDF]

Home page
 Biol. Reprod.Home page
B. Roy, B. Sicotte, M. Brochu, and J. St-Louis
Modulation of Calcium Mobilization in Aortic Rings of Pregnant Rats:Contribution of Extracellular Calcium and of Voltage-Operated Calcium Channels
Biol Reprod, April 1, 1999; 60(4): 979 - 988.
[Abstract] [Full Text]

Home page
 J. Pharmacol. Exp. Ther.Home page
M. Tosun, R. J. Paul, and R. M. Rapoport
Coupling of Store-Operated Ca++ Entry to Contraction in Rat Aorta
J. Pharmacol. Exp. Ther., May 1, 1998; 285(2): 759 - 766.
[Abstract] [Full Text]

Home page
 J. Pharmacol. Exp. Ther.Home page
M. Tosun, R. J. Paul, and R. M. Rapoport
Role of Extracellular Ca++ Influx via L-Type and Non-L-Type Ca++ Channels in Thromboxane A2 Receptor-Mediated Contraction in Rat Aorta
J. Pharmacol. Exp. Ther., March 1, 1998; 284(3): 921 - 928.
[Abstract] [Full Text]


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 1987 by the American Society for Pharmacology and Experimental Therapeutics.