Opposite effects of Gα_i2 or Gα_i3 deficiency on reduced basal density and attenuated β-adrenergic response of ventricular Ca²⁺ currents in myocytes of mice overexpressing the cardiac β₁-adrenoceptor.

ABSTRACT: Ca²⁺ currents (I_CaL) carried by ventricular L-type Ca²⁺ channels (LTCC) are altered in failing hearts, and increased LTCC activity is discussed as a cause of cardiomyopathy. We have shown that lack of the inhibitory G-protein isoform Gα_i3 improves cardiac outcome and survival in a murine heart-failure model of cardiac β₁-adrenoceptor (β₁-AR) overexpression (β₁-tg), while lack of the Gα_i2 isoform was detrimental in the same heart-failure model. Given the potential role of LTCC and their modulation by β-adrenergic signalling, we now analysed ventricular I_CaL in β₁-tg mice and in β₁-tg mice lacking either Gα_i2 or Gα_i3. Using the patch-clamp technique,

SUBMITTER: Katnahji N 

PROVIDER: S-EPMC12449356 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature