Hypertrophy alters effect of Ins(1,4,5)P3 on Ca2+ release in skinned rat heart muscle

N. Furukawa, A. L. BassetT, T. Furukawa, R. J. Myerburg, S. Kimura

Research output: Contribution to journalArticle

11 Scopus citations

Abstract

The effects of D-myo-inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] on the ability of the sarcoplasmic reticulum (SR) to accumulate and release Ca2+ and on the Ca2+ sensitivity of the contractile proteins were investigated using chemically (saponin) skinned cardiac fibers (60-120 μm diam) obtained from normal and pressure-overloaded hypertrophied rat left ventricles. Left ventricular pressure overload was induced by partial ligation of the abdominal aorta 3-6 wk before study. Age- and weight-matched normal rats served as controls. Pressure overload increased the left ventricular weight-to-body weight ratio by 45%. Ins(1,4,5)P3 at a concentration of 10 μM did not change the Ca2+-tension relationship at Ca2+ concentrations of 10-7 to 10-5 M in either normal or hypertrophied fibers. Ins(1,4,5)P3 also did not influence Ca2+ uptake by the SR in either normal or hypertrophied fibers. Ins(1,4,5)P3 did not induce Ca2+ release from the SR directly in either group. However, pretreatment with Ins(1,4,5)P3 enhanced the 5 mM caffeine-induced Ca2+ release by 80.5 ± 22.7% in normal fibers but not in hypertrophied fibers. We conclude that Ins(1,4,5)P3 enhances, rather than directly induces, SR Ca2+ release in normal rat hearts and that sustained pressure overload diminishes the response of the SR Ca2+-release system to Ins(1,4,5)P3, an action that may be partly responsible for contractile dysfunction in cardiac hypertrophy.

Original languageEnglish (US)
Pages (from-to)H1612-H1618
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume260
Issue number5 29-5
DOIs
StatePublished - Jan 1 1991

Keywords

  • Calcium sensitivity
  • Calcium uptake
  • Chronic pressure overload
  • Sarcoplasmic reticulum

ASJC Scopus subject areas

  • Physiology

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