Regular ArticleDesensitization of cardiac β -adrenoceptor signaling with heart failure produced by myocardial infarction in the rat. Evidence for the role of Gi but not Gs or phosphorylating proteins
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β<inf>3</inf>-adrenergic receptor activation induces TGFβ1 expression in cardiomyocytes via the PKG/JNK/c-Jun pathway
2018, Biochemical and Biophysical Research CommunicationsThe functional activity of inhibitory G protein (G<inf>i</inf>) is not increased in failing heart ventricle
2013, Journal of Molecular and Cellular CardiologyCitation Excerpt :In guinea-pig cardiomyocytes chronically treated with noradrenaline and in human cardiomyocytes from heart failure patients, PTX restored the maximal fractional cell shortening to βAR stimulation [30]. In a study directly measuring contractile force, PTX treatment partially restored the attenuated βAR-mediated inotropic response in both left atria and ventricular papillary muscles in a post-infarction rat model of heart failure [15]. Based on the aforementioned reports, the prevailing inference has been that increased Gi protein activity contributes to the reduced βAR responsiveness in the failing heart.
Role of PKC-ζ in NADPH oxidase-PKCα-G<inf>i</inf>α axis dependent inhibition of β-adrenergic response by U46619 in pulmonary artery smooth muscle cells
2013, Archives of Biochemistry and BiophysicsCitation Excerpt :Secondly, to ascertain involvement of the PKC isozyme(s) in attenuating isoproterenol stimulated of adenyl cyclase activity in the cells. And, thirdly, in view of a previous report that in pulmonary artery endothelial cells pretreatment with pertussis toxin eliminates the protein kinase C activator, phorbol ester caused attenuation of isoproterenol stimulated adenyl cyclase activity [5]; and also that Gi has been shown to play an important role in decreased β-adrenergic responsiveness in a rat model of myocardial infarction [30], we tested the hypothesis that U46619 caused inhibition of isoproterenol stimulated adenyl cyclase activity occurs via phosphorylation of Gi by PKC in the pulmonary smooth muscle cells. Our present study that Tp receptor activation by U46619 caused attenuation of isoprotereol stimulated adenyl cyclase activity occurs markedly, but not completely, via PKC-ζ dependent activation of NADPH oxidase with subsequent stimulation of PKC-α activity in the smooth muscle cells.
Testosterone modulation of cardiac β-adrenergic signals in a rat model of heart failure
2011, General and Comparative EndocrinologyFunctional remodeling in post-myocardial infarcted rats: Focus on beta-adrenoceptor subtypes
2006, Journal of Molecular and Cellular CardiologyCitation Excerpt :In this PMI rat model, PTX treatment (that is, removal of the inhibitory activity of Gi), restored the response to β1AR to the extent measured in SHAM rats. Thus, overexpression of Gi seems to exert a major, independent role in the attenuation of the βAR response in severe cardiac failure [11,26]. In this line, previous results obtained in Gαq hypertrophic mouse hearts and in HEK293 cells overexpressing Gαi2 suggest that the increase in Gi has a contribution to the βAR signaling defect, but not to the response to forskolin [36].
Emerging concepts and therapeutic implications of β-adrenergic receptor subtype signaling
2005, Pharmacology and Therapeutics
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Please address all correspondence to: Professor Roger J. Summers, Department of Pharmacology, Monash University, Wellington Road, Clayton, Victoria, Australia, 3168. Email: [email protected]