JPET

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


     

This Article
Right arrow Full Text
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
Right arrow Citation Map
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 Temsah, R. M.
Right arrow Articles by Dhalla, N. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Temsah, R. M.
Right arrow Articles by Dhalla, N. S.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*ATENOLOL
*CALCIUM COMPOUNDS
*CALCIUM, ELEMENTAL
*PROPRANOLOL HYDROCHLORIDE
Medline Plus Health Information
*Cardiomyopathy

Vol. 293, Issue 1, 15-23, April 2000

Effect of beta -Adrenoceptor Blockers on Sarcoplasmic Reticular Function and Gene Expression in the Ischemic-Reperfused Heart1

Rana M. Temsah, Chadwyn Dyck, Thomas Netticadan, Donald Chapman, Vijayan Elimban and Naranjan S. Dhalla

Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre; and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada

Although beta -adrenoceptor (beta -AR) blockers are used for the treatment of ischemic heart disease, the mechanisms of their beneficial actions have not been fully elucidated. In view of the role of sarcoplasmic reticular (SR) abnormalities in cardiac dysfunction due to ischemia-reperfusion (I/R), we examined the effects of beta -AR blockers on the I/R-induced changes in SR Ca2+ uptake and release, as well as the protein contents and gene expression of ryanodine receptor, SR Ca2+-pump, phospholamban, and calsequestrin. I/R in isolated rat hearts was induced by stopping the perfusion for 30 min and then reperfusing the ischemic hearts for 60 min. Hearts were treated with or without 10 µM atenolol, a beta 1-specific blocker, or 10 µM propranolol, a nonspecific beta -blocker, 10 min before inducing ischemia as well as during the reperfusion period. I/R depressed cardiac performance, SR Ca2+ uptake, and Ca2+ release activities, protein contents, as well as Ca2+/calmodulin-dependent protein kinase and cAMP-dependent protein kinase-mediated phosphorylations, significantly. The mRNA levels for SR Ca2+ pump, ryanodine receptors, phospholamban, and calsequestrin were also reduced by I/R. All these changes due to I/R were partially prevented by beta -AR blocker treatment. The results indicate that the beneficial effects of beta -AR blockers on cardiac performance in the I/R hearts may be related to the prevention of changes in SR Ca2+ uptake and release activities, protein contents, as well as Ca2+/calmodulin-dependent protein kinase and cAMP-dependent protein kinase phosphorylations of SR proteins. On the other hand, the protection of I/R-induced alterations in mRNA levels for SR proteins by beta -AR blockers suggests cardiac SR gene expression as a molecular site of their cardioprotective action.

1 This study was supported by a grant from the Medical Research Council of Canada (MRC Group in Experimental Cardiology. Rana M. Temsah received studentship award of the University of Manitoba; Chadwyn Dyck received support from the B. Sc. (Med) program at the Faculty of Medicine. Dr. Naranjan S. Dhalla holds MRC/Pharmaceutical Research and Development Chair in Cardiovascular Research supported by Merck Frosst, Canada.

0022-3565/00/2931-0015$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 2000 by The American Society for Pharmacology and Experimental Therapeutics


This article has been cited by other articles:


Home page
 EndocrinologyHome page
D. X. Tishkoff, K. A. Nibbelink, K. H. Holmberg, L. Dandu, and R. U. Simpson
Functional Vitamin D Receptor (VDR) in the T-Tubules of Cardiac Myocytes: VDR Knockout Cardiomyocyte Contractility
Endocrinology, February 1, 2008; 149(2): 558 - 564.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
H. M. Yeung, G. M. Kravtsov, K. M. Ng, T. M. Wong, and M. L. Fung
Chronic intermittent hypoxia alters Ca2+ handling in rat cardiomyocytes by augmented Na+/Ca2+ exchange and ryanodine receptor activities in ischemia-reperfusion
Am J Physiol Cell Physiol, June 1, 2007; 292(6): C2046 - C2056.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
C. Ballard-Croft, D. Carlson, D. L. Maass, and J. W. Horton
Burn trauma alters calcium transporter protein expression in the heart
J Appl Physiol, October 1, 2004; 97(4): 1470 - 1476.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
M. Stange, L. Xu, D. Balshaw, N. Yamaguchi, and G. Meissner
Characterization of Recombinant Skeletal Muscle (Ser-2843) and Cardiac Muscle (Ser-2809) Ryanodine Receptor Phosphorylation Mutants
J. Biol. Chem., December 19, 2003; 278(51): 51693 - 51702.
[Abstract] [Full Text] [PDF]

Home page
 Canadian J. AnesthesiaHome page
S. Kurosawa, N. Kanaya, Y. Niiyama, M. Nakayama, S. Fujita, and A. Namiki
Landiolol, esmolol and propranolol protect from ischemia/reperfusion injury in isolated guinea pig hearts: [Le landiolol, l'esmolol et le propranolol protegent des lesions resultant de l'ischemie/reperfusion dans des coeurs de cobaye isoles]
Can J Anesth, May 1, 2003; 50(5): 489 - 494.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
R. M. Temsah, T. Netticadan, K.-I. Kawabata, and N. S. Dhalla
Lack of both oxygen and glucose contributes to I/R-induced changes in cardiac SR function
Am J Physiol Cell Physiol, October 1, 2002; 283(4): C1306 - C1312.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
R. M. Temsah, K. Kawabata, D. Chapman, and N. S. Dhalla
Preconditioning prevents alterations in cardiac SR gene expression due to ischemia-reperfusion
Am J Physiol Heart Circ Physiol, April 1, 2002; 282(4): H1461 - H1466.
[Abstract] [Full Text] [PDF]

Home page
 Br J AnaesthHome page
M. Zaugg, M. C. Schaub, T. Pasch, and D. R. Spahn
Modulation of {beta}-adrenergic receptor subtype activities in perioperative medicine: mechanisms and sites of action
Br. J. Anaesth., January 1, 2002; 88(1): 101 - 123.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
R. Tupling, H. Green, G. Senisterra, J. Lepock, and N. McKee
Effects of 4-h ischemia and 1-h reperfusion on rat muscle sarcoplasmic reticulum function
Am J Physiol Endocrinol Metab, October 1, 2001; 281(4): E867 - E877.
[Abstract] [Full Text] [PDF]


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

Copyright © 2000 by the American Society for Pharmacology and Experimental Therapeutics.