NDLI: Attenuation of changes in sarcoplasmic reticular gene expression in cardiac hypertrophy by propranolol and verapamil

Content Provider	Springer Nature Link
Author	Takeo, Satoshi Elmoselhi, Adel B. Goel, Raj Sentex, Emmanuelle Wang, Jingwei Dhalla, Naranjan S.
Copyright Year	2000
Abstract	The effects of propranolol and verapamil on contractile dysfunction, subcellular remodeling and changes in gene expression in cardiac hypertrophy due to pressure overload were examined. Rats were subjected to banding of the abdominal aorta and then treated with either propranolol (10 mg/kg daily), verapamil (5 mg/kg daily) or vehicle for 8 weeks after the surgery. Depression of the left ventricular function in the hypertrophied heart was associated with decreases in myofibrillar and myosin CA$^{2+}$ ATPase activities as well as Ca$^{2+}$-pump and Ca$^{2+}$-release activities of the sarcoplasmic reticulum (SR). The level of a-myosin heavy chain (α-MHC) mRNA was decreased while that of β-MHC mRNA was increased in the pressure-overloaded heart. The level of SR Ca$^{2+}$-pump ATPase (SERCA2) mRNA and protein content for SERCA2 were decreased in the pressure overloaded heart. Treatment of the hypertrophied animals with propranolol or verapamil resulted in preservation of the left ventricular function and prevention of the subcellular alterations. Shift in the α- and β-MHC mRNA levels and changes in the expression in SERCA2 mRNA level and protein content were also attenuated by these treatments. The results suggest that blockade of β-adrenoceptors or voltage-dependent calcium channels normalizes the cardiac gene expression, prevents subcellular remodeling and thus attenuates heart dysfunction in rats with cardiac hypertrophy. Furthermore, both cardiac β-adrenoceptors and L-type Ca$^{2+}$-channels may be involved in the genesis of cardiac hypertrophy due to pressure overload.
Starting Page	111
Ending Page	118
Page Count	8
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	213
Issue Number	1-2
e-ISSN	15734919
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2000-01-01
Publisher Place	Boston
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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