Targeting the Receptor-G q Interface to Inhibit in Vivo Pressure Overload Myocardial Hypertrophy

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Abstract
Hormones and neurotransmitters may mediate common responses through receptors that couple to the same class of heterotrimeric guanine nucleotide–binding (G) protein. For example, several receptors that couple to G q class proteins can induce cardiomyocyte hypertrophy. Class-specific inhibition of G q -mediated signaling was produced in the hearts of transgenic mice by targeted expression of a carboxyl-terminal peptide of the α subunit Gα q . When pressure overload was surgically induced, the transgenic mice developed significantly less ventricular hypertrophy than control animals. The data demonstrate the role of myocardial G q in the initiation of myocardial hypertrophy and indicate a possible strategy for preventing pathophysiological signaling by simultaneously blocking multiple receptors coupled to G q .