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G-protein and Membrane Signaling in Cardiovascular Disease

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Abstract

Guanine nucleotide regulatory proteins (G-proteins) play a key role in the regulation of various signal transduction systems, which are implicated in the modulation of a variety of physiological functions such as platelet functions, including platelet aggregation, secretion, and clot formation, and cardiovascular functions, including arterial tone and reactivity. Several abnormalities in adenylyl cyclase activity, cAMP levels, and G-protein levels have shown to be responsible for the altered cardiac performance and vascular functions observed in cardiovascular disease states. The enhanced or unaltered levels of inhibitory G-proteins(Giα-2 and Giα-3) and mRNA have been reported in different models of hypertension, whereas Gsα levels were shown to be unaltered. These changes in G-protein were associated with functions. The enhanced levels of Giα proteins precede the development of blood pressure and suggest that over expression of Gi proteins may be one of the contributing factors for the pathogenesis of hypertension. On the other hand, the levels of Gsα and not of Giα proteins were decreased in volume- or pressure-overload hypertrophy. The responsiveness of adenylyl cyclase to β-adrenergic agonists was also attenuated. Similarly, is chemia was shown to be associated with decreased, increased,or unaltered levels of Gsα, with decreased levels of Giα, and with decreased responsiveness of adenylyl cyclase to various stimuli such as β-adrenergic agonists, guanine nucleotides, forskolin, etc. Thus,the altered levels of G-proteins and cAMP levels may be responsible for the impaired cardiovascular functions observed in hypertension, hypertrophy,and cardiac failure.

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  1. Department of Physiology and Groupe de recherche sur le système nerveux autonome (GRSNA), University of Montreal, Montreal, Quebec, Canada

    Madhu B. Anand-Srivastava

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Anand-Srivastava, M.B. G-protein and Membrane Signaling in Cardiovascular Disease. Heart Fail Rev 2, 85–94 (1997). https://doi.org/10.1023/A:1009767810044

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