REGULATION OF MYOSIN ISOZYME EXPRESSION BY VITAMIN-D-3 DEFICIENCY AND 1,25-DIHYDROXYVITAMIN-D-3 IN THE RAT-HEART

In this report, we demonstrate a significant inverse correlation between contractility and serum 1,25-dihydroxyvitamin D-3 [1,25-(OH)(2)D-3] levels and no correlation between contractility and serum levels of calcium, phosphate, or PTH. We also examined myosin isozyme distribution in vitamin DB-deficient rats, because myosin isozyme distribution can alter contractility. There was a significant increase in the levels of the V-1 myosin isozyme in animals raised on a vitamin D-3-deficient diet that maintained normal serum calcium and phosphate levels. There was no difference in the relative myosin isozyme distribution in animals raised on a hypocalcemia-yielding vitamin D-3-deficient diet us. animals raised on a control diet. As increased contractility has been observed in both groups of vitamin D-3-deficient animals, a shift in myosin isozyme distribution cannot solely explain the increase in contractility previously observed in the vitamin D-3-deficient rat heart. To determine whether 1,25-(OH)(2)D-3 directly regulates myosin isozyme levels, we analyzed myosin isozyme distribution in primary cultures of ventricular myocytes. We found that 1,25-(OH)(2)D-3 reduces total myosin levels, but does not alter myosin isozyme distribution. Thus, we show that the influence of vitamin D-3 status on myosin isozyme expression in the intact rat involves a complex regulatory system of direct and indirect effects.