EFFECT OF PARATHYROID-HORMONE ON MYOCARDIAL ENERGY-METABOLISM IN THE RAT

This study examined the effect of parathyroid hormone (PTH) on myocardial energy production, transfer, and utilization. Rats (150 to 200 g) were injected with 1-84 PTH, 200 U/day i.p., or 1-34 PTH, 200 or 300 U/day i.p., for 4 days. Control animals received the vehicle only. The effect of the simultaneous administration of Ca channel blocker, verapamil, was also exmained. Myocardial contents of Pi [inorganic phosphorus] ATP, and CP (creative phosphate) were significantly (P < 0.01) lower in the 1-84 PTH-treated rats than in control animals. Both 1-84 PTH and 1-34 significantly (P < 0.01) reduced mitochondrial oxygen consumption without altering ADP:O ratio indicating reduced phosphorylation. The 1-84 and 1-34 PTH significantly (P < 0.01) reduced the activities of mitochondrial and myofibrillar creatine phosphokinase and 1-84 PTH inhibited (P < 0.01) the activities of mitochondrial Mg ATPase and those of myofibrillar Ca ATPase. There were significant (P < 0.01) increments in myocardial 45Ca and in total Ca content in 1-84 PTH-treated rats. Verapamil abolished all the effects of 1-84 PTH. Similarly, inactiviation of 1-84 PTH abolished its effects. Treatament with 1-84 PTH for 10 days was associated with a significant decrease in cardiac index and mean arterial pressure. Data demonstrate that both 1-84 and 1-34 PTH impair energy production, transfer, and utilization. These biochemical derangements, if maintained, produce a decrease in cardiac index. It appears that the enhanced entry and the accumulation of Ca in the myocardium, either directly and/or indirectly, are responsible for the action of PTH on energy metabolism of the heart.