Targeted inactivation of Galpha(i2) or Galpha(i3) in mice did not alter basal cardiac function or sensitivity to beta-adrenergic stimulation compared to wild-type mice.
Does targeted inactivation of Galpha(i2) or Galpha(i3) alter basal cardiac function or sensitivity to beta-adrenergic stimulation in nonpathological myocardium?
Inhibitory G proteins Galpha(i2) and Galpha(i3) do not play an observable role in mediating basal cardiac function or sensitivity to beta-adrenergic stimulation in nonpathological myocardium.
Inhibitory Galpha(i) protein increases in the myocardium during hypertrophy and has been associated with beta-adrenergic receptor (beta-AR) desensitization, contractile dysfunction, and progression of cardiac disease. The role of Galpha(i) proteins in mediating basal cardiac function and beta-AR response in nonpathological myocardium, however, is uncertain. Transgenic mice with targeted inactivation of Galpha(i2) or Galpha(i3) were examined for in vivo cardiac function with the use of conscious echocardiography and for ex vivo cardiac response to inotropic stimulation with the use of Langendorff blood-perfused isolated hearts and adult ventricular cardiomyocytes. Echocardiography revealed that percent fractional shortening and heart rate were similar among wild-type, Galpha(i2)-null, and Galpha(i3)-null mice. Comparable baseline diastolic and contractile performance was also observed in isolated hearts and isolated ventricular myocytes from wild-type mice and mice lacking Galpha(i) proteins. Isoproterenol infusion enhanced diastolic and contractile performance to a similar degree in wild-type, Galpha(i2)-null, and Galpha(i3)-null mice. These data demonstrate no observable role for inhibitory G proteins in mediating basal cardiac function or sensitivity to beta-AR stimulation in nonpathological myocardium.
Jain et al. (Thu,) conducted a other in Nonpathological myocardium. Targeted inactivation of Galpha(i2) or Galpha(i3) vs. Wild-type mice was evaluated on In vivo cardiac function and ex vivo cardiac response to inotropic stimulation. Targeted inactivation of Galpha(i2) or Galpha(i3) in mice did not alter basal cardiac function or sensitivity to beta-adrenergic stimulation compared to wild-type mice.