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—Hypertensive cardiac  hypertrophy and myocardial infarction (MI) are clinically  relevant risk factors for heart failure. There is no specific  information addressing signaling alterations in the sequence of  hypertrophy and post-MI remodeling. To investigate  alterations in β-adrenergic receptor G-protein signaling in  ventricular remodeling with pre-existing  hypertrophy, MI was induced by coronary artery  ligation in Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats  (SHR). Ten weeks after the induction of MI, the progression of left  ventricular dysfunction and increases in plasma atrial  natriuretic peptide (ANP) and cardiac ANP mRNA were more  pronounced in SHR than WKY. In addition, the impaired contractile  response to β-adrenergic stimulation was observed in the noninfarcted  papillary muscle isolated from SHR. Immunochemical Gsα protein and β-adrenoceptor density were not significantly altered by  MI in both strains. However, immunochemical Giα was  increased (1.5-fold) in the noninfarcted left ventricle of the SHR in  which infarction had been induced when compared with that in SHR that  underwent sham operation. This increase was observed especially in rats  with a high plasma ANP level. Furthermore, there was a positive  correlation between Giα and the extent of post-MI  remodeling in WKY. A similar correlation between Giα and  the extent of hypertensive hypertrophy was observed in SHR.  In conclusion, the vulnerability of hypertrophied hearts to  ischemic damage is greater than that of normotensive hearts. An  increase in Giα could be one mechanism involved in the  transition from cardiac hypertrophy to cardiac failure when  chronic pressure overload and loss of contractile mass from  ischemic heart disease coexist.

Increase in G iα Protein Accompanies Progression of Post-Infarction Remodeling in Hypertensive Cardiomyopathy

Increase in G _iα Protein Accompanies Progression of Post-Infarction Remodeling in Hypertensive Cardiomyopathy