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Am J Physiol Cell Physiol 279: C1455-C1463, 2000;
0363-6143/00 $5.00
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Vol. 279, Issue 5, C1455-C1463, November 2000

Impaired Gsalpha and adenylyl cyclase cause beta -adrenoceptor desensitization in chronically hypoxic rat hearts

Jian-Ming Pei1, Xiao-Chun Yu1, Man-Lung Fung1,2, Jing-Jun Zhou1, Chi-Sing Cheung1, Nai-Sum Wong3, Maurrice-Ping Leung2,4, and Tak-Ming Wong1,2

Departments of 1 Physiology, 3 Biochemistry, and 4 Pediatrics; and 2 Institute of Cardiovascular Sciences and Medicine, Faculty of Medicine, University of Hong Kong, Hong Kong, China

The effects of beta -adrenoceptor stimulation with isoproterenol on electrically induced contraction and intracellular calcium ([Ca2+]i) transient, and cAMP in myocytes from both hypertrophied right and nonhypertrophied left ventricles of rats exposed to 10% oxygen for 4 wk, were significantly attenuated. The increased [Ca2+]i transient in response to cholera toxin was abolished, whereas increased cAMP after NaF significantly attenuated. The biologically active isoform, Gsalpha -small (45 kDa), was reduced while the biologically inactive isoform, Gsalpha -large (52 kDa), increased. The increased electrically induced [Ca2+]i transient and cAMP with 10-100 µM forskolin were significantly attenuated in chronically hypoxic rats. The content of Gialpha 2, the predominant isoform of Gi protein in the heart, was unchanged. Results indicate that impaired functions of Gs protein and adenylyl cyclase cause beta -adrenoceptor desensitization. The impaired function of the Gs protein may be due to reduced Gsalpha -small and/or increased Gsalpha -large, which does not result from changes in Gi protein. Responses to all treatments were the same for right and left ventricles, indicating that the impaired cardiac functions are not secondary to cardiac hypertrophy.

G protein; cardiac hypertrophy


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