NDLI: Role of cardiac renin-angiotensin system in sarcoplasmic reticulum function and gene expression in the ischemic-reperfused heart

Content Provider	Springer Nature Link
Author	Takeo, Satoshi Nasa, Yoshihisa Tanaka, Kouichi Yamaguchi, Fuminari Yabe, Ken ichi Hayashi, Hideki Dhalla, Naranjan S.
Copyright Year	2000
Abstract	The aim of this study was to explore the possible participation of cardiac renin-angiotensin system (RAS) in the ischemia-reperfusion induced changes in heart function as well as Ca$^{2+}$-handling activities and gene expression of cardiac sarcoplasmic reticulum (SR) proteins. The isolated rat hearts, treated for 10 min without and with 30 μM captopril or 100 μM losartan, were subjected to 30 min ischemia followed by reperfusion for 60 min and processed for the measurement of SR function and gene expression. Attenuated recovery of the left ventricular developed pressure (LVDP) upon reperfusion of the ischemic heart was accompanied by a marked reduction in SR Ca$^{2+}$-pump ATPase, Ca$^{2+}$-uptake and Ca$^{2+}$-release activities. Northern blot analysis revealed that mRNA levels for SR Ca$^{2+}$-handling proteins such as Ca$^{2+}$-pump ATPase (SERCA2a), ryanodine receptor, calsequestrin and phospholamban were decreased in the ischemia-reperfused heart as compared with the non-ischemic control. Treatment with captopril improved the recovery of LVDP as well as SR Ca$^{2+}$-pump ATPase and Ca$^{2+}$-uptake activities in the postischemic hearts but had no effect on changes in Ca$^{2+}$-release activity due to ischemic-reperfusion. Losartan neither affected the changes in contractile function nor modified alterations in SR Ca$^{2+}$-handling activities. The ischemia-reperfusion induced decrease in mRNA levels for SR Ca$^{2+}$-handling proteins were not affected by treatment with captopril or losartan. The results suggest that the improvement of cardiac function in the ischemic-reperfused heart by captopril is associated with the preservation of SR Ca$^{2+}$-pump activities; however, it is unlikely that this action of captopril is mediated through the modification of cardiac RAS. Furthermore, cardiac RAS does not appear to contribute towards the ischemia-reperfusion induced changes in gene expression for SR Ca$^{2+}$-handling proteins.
Starting Page	227
Ending Page	235
Page Count	9
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	212
Issue Number	1-2
e-ISSN	15734919
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2000-01-01
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Cardiology Medical Biochemistry Oncology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Clinical Biochemistry Molecular Biology

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