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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