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Prolonged exposure of cells to adenylyl cyclase stimulatory hormonal factors can cause an increase in the level of membrane inhibitory G protein (Gi) alpha-subunits, while inhibitory receptor agonists have been reported to induce the opposite response. As studied in cultured rat cardiomyocytes, the beta-adrenoceptor-induced increase in the level of Gi alpha proteins is protein synthesis-dependent, is apparently not accompanied by an increase in G protein beta-subunits and results in a decreased adenylyl cyclase responsiveness. On the other hand, a decrease in Gi alpha level apparently results in sensitization of adenylyl cyclase stimulation. These data suggest that the up- or down-regulation of the level and activity of Gi protein alpha-subunits is a rather general cellular response, providing an intracellular negative feedback control against prolonged receptor activation.
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