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1 Division of Physiology and
2 Department of Oral Biology,
The involvement of reduced thyroxine level
in the emergence of heat acclimation-induced negative lusitropic effect
was examined. Experiments were carried out on
1) control rat hearts maintained at
24 ± 1°C (C); 2) rat hearts
acclimated at 34°C for 1 mo (AC); 3) AC-euthyroid rat hearts, via
administration of thyroxine in the drinking water (AT); and
4) hypothyroid rat hearts,
maintained at 24 ± 1°C, via administration of thiouracil in the
drinking water (CP). Systolic pressure and velocities of contraction
(dP/dt · P) and
relaxation
(
dP/dt · P)
were measured using the Langendorff perfusion system. The steady-state
levels of Ca2+-ATPase and
phospholamban mRNAs and the expression of the encoded proteins
Ca2+-ATPase (SERCA) and
phospholamban (PLB) were measured, using semi-quantitative RT-PCR and
Western immunoblotting, respectively. Rat thyroxine levels were
measured using RIA. Heat acclimation, which brought about a reduced
thyroxine level, led to downregulation of
Ca2+-ATPase mRNA expression and
translation and upregulation of phospholamban mRNA and PLB.
Consequently, the PLB-to-SERCA ratio (PLB/SERCA) of the AC hearts
showed a significant increase. These changes, as well as the greater
pressure generation and the reduced
dP/dt · P and
dP/dt · P
observed in AC hearts were blunted in the AT hearts. Our data suggest
that sustained heat acclimation-induced low thyroxine level has a
decisive effect on the contractile machinery of the AC heart. Elevated
PLB/SERCA apparently explains the negative lusitropic effect observed
in these hearts.
phospholamban; calcium adenosine 5'-triphosphatase; mRNA; Ca2+ regulatory proteins; thyroxine; heart; cardiac relaxation
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