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Am J Physiol Heart Circ Physiol 274: H385-H396, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 2, H385-H396, February 1998

Troponin I phosphorylation and myofilament calcium sensitivity during decompensated cardiac hypertrophy

Bradley K. McConnell1,2, Christine Schomisch Moravec1,2,3, and Meredith Bond1,2

1 Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland 44106; and 2 Department of Molecular Cardiology, Lerner Research Institute, 3 Center for Anesthesiology Research, Cleveland Clinic Foundation, Cleveland, Ohio 44195

We have measured myocyte cell shortening, troponin-I (Tn-I) phosphorylation, Ca2+ dependence of actomyosin adenosinetriphosphatase (ATPase) activity, adenosine 3',5'-cyclic monophosphate (cAMP) levels, and myofibrillar isoform expression in the spontaneously hypertensive rat (SHR) during decompensated cardiac hypertrophy (76 wk old) and in age-matched Wistar-Kyoto rat (WKY) controls. The decreased inotropic response to beta -adrenergic stimulation previously observed in myocytes from 26-wk-old SHR was further reduced at 76 wk of age. In response to beta -adrenergic stimulation, Tn-I phosphorylation was greater in the 76-wk-old SHR than in the WKY, although cAMP-dependent protein kinase A (PKA)-dependent Tn-I phosphorylation in the SHR did not increase with progression from compensated (26 wk) to decompensated (76 wk) hypertrophy. We also observed a dissociation between the increased PKA-dependent Tn-I phosphorylation and decreased cAMP levels in the 76-wk-old SHR versus WKY during beta -adrenergic stimulation. Baseline Tn-I phosphorylation was significantly reduced in 76-wk-old SHR versus WKY and was associated with decreased basal cAMP levels and increased Ca2+ sensitivity of actomyosin ATPase activity. The change in myofilament Ca2+ sensitivity during beta -adrenergic stimulation in the 76-wk-old SHR (0.65 pCa units) was over twofold greater than in the 76-wk-old WKY (0.30 pCa units). We also determined whether embryonic troponin T isoforms were reexpressed in decompensated hypertrophy and observed significant reexpression of the embryonic cardiac troponin T isoforms in the 76-wk-old SHR. The significant decrease in Ca2+ sensitivity with beta -adrenergic stimulation in 76-wk-old SHR may contribute to the severely impaired inotropic response during decompensated hypertrophy in the SHR.

spontaneously hypertensive rat; inotropic response; adenosine 3',5'-cyclic monophosphate-dependent protein kinase; beta -adrenergic stimulation; actomyosin adenosinetriphosphatase activity


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