Alterations in the Inotropic Responses to Forskolin and Ca<SUP>2+</SUP> and Reduced Gene Expressions of Ca<SUP>2+</SUP>-Signaling Proteins Induced by Chronic Volume Overload in Rabbits

  • Takahashi Noriko
    The First Department of Internal Medicine, Yamagata University School of Medicine, Yamagata, Japan
  • Atsumi Hiroyuki
    The First Department of Internal Medicine, Yamagata University School of Medicine, Yamagata, Japan
  • Nakada Shigekazu
    The First Department of Internal Medicine, Yamagata University School of Medicine, Yamagata, Japan
  • Takeishi Yasuchika
    The First Department of Internal Medicine, Yamagata University School of Medicine, Yamagata, Japan
  • Tomoike Hitonobu
    The First Department of Internal Medicine, Yamagata University School of Medicine, Yamagata, Japan

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説明

Volume overload results in eccentric cardiac hypertrophy, but it is still unknown how this mechanical overload modulates the inotropic response to exogenous Ca2+ or adenylyl cyclase stimulation. Inotropic responsiveness in vivo and the levels of gene expression of Ca2+ signaling proteins were studied in rabbit hearts hypertrophied as a result of volume overload at 4 and 12 weeks after arteriovenous shunt formation. In sham-operated control rabbits, left ventricular (LV)+dP/dt was augmented in response to graded doses of CaCl2. Dose-related changes of LV+dP/dt to CaCl2 were attenuated significantly in shunt rabbits with volume overload. Forskolin dose-dependently augmented LV+dP/dt in sham rabbits, which was also attenuated significantly in rabbits with volume overload. The mRNA levels of dihydropyridine receptor, Na+/Ca2+ exchanger, sarcoplasmic reticulum Ca2+-ATPase, and ryanodine receptor decreased significantly at 4 and 12 weeks in the volume-overload rabbits compared with the sham rabbits, but the mRNA levels of phospholamban and calsequestrin remained unchanged. Chronic volume overload alters contractile responsiveness to Ca2+ or adenylyl cyclase stimulation, and downregulation of steady state mRNA levels of Ca2+ signaling proteins might be, at least in part, related to this pathologic process.

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