Effects of parathyroid hormone on oxidative phosphorylation of heart mitochondria.

Abstract

In an effort to understand the mechanism of action of parathyroid hormone (PTH) on the myocardium, we examined the effect of PTH on the function of isolated heart mitochondria. The hormone inhibited mitochondrial respiration in the presence of malate or beta-hydroxybutyrate but not succinate as substrates. It also inhibited phosphorylation and uncoupled oxidative phosphorylation. These effects of PTH were dose dependent and occurred only in the presence of calcium. A change in calcium concentration from zero to 2 mM did not affect mitochondrial function. PTH also stimulated mitochondrial ATPase. The inhibitory effect of PTH on mitochondrial respiration and on oxidative phosphorylation would result in decreased ATP synthesis and, hence, reduced availability of ATP. Such a sequence of events may provide an explanation for a potential long-term adverse effect of the hormone on the myocardium.