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Vol. 293, Issue 1, 15-23, April 2000
-Adrenoceptor Blockers on Sarcoplasmic Reticular
Function and Gene Expression in the Ischemic-Reperfused
Heart1
Institute of Cardiovascular Sciences, St. Boniface General Hospital
Research Centre; and Department of Physiology, Faculty of Medicine,
University of Manitoba, Winnipeg, Canada
Although 
-adrenoceptor (-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 -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
1-specific blocker, or 10 µM propranolol, a nonspecific -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 -AR blocker treatment. The results
indicate that the beneficial effects of -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 -AR blockers suggests cardiac SR
gene expression as a molecular site of their cardioprotective action.
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