Effect of Epinephrine on Parathyroid Hormone Secretion in Calves

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Abstract
The effect of epinephrine on parathyroid hormone (PTH) secretion rate and the molecular nature of immunoreactivity in parathyroid venous blood was assessed in seven anesthetized calves. PTH secretion rate was measured by a technique which involved RIA of parathyroid venous blood that was collected during timed intervals and measured volumetrically. The molecular nature of immunoreactivity in parathyroid venous plasma was evaluated by gel column chromatography and RIAs which recognized specific regions of the PTH molecule, i.e. the amino-terminus or carboxyl-terminus. Plasma calcium concentration was measured by chelometric titration. Epinephrine HCI was infused iv into a normocalcemic calf at rates of 0.025, 0.05, 0.10, 0.25, and 0.40 μg/kg-min. PTH secretion rate progressively increased in response to increased rates of infusion until a near maximal secretion rate was attained at an infusion rate of 0.25 μg/kg-min. Epinephrine HCI was infused iv into five calves at a rate of 0.25 μg/kg-min during and after induced alterations of plasma calcium concentration. Epinephrine infusion was accompanied by an increase in PTH secretion rate during normocalcemia and hypocalcemia, but the response was either greatly diminished or absent during hypercalcemia. The magnitude of the increase in secretion rate above control values was inversely related to plasma calcium concentration. The duration of response to epinephrine was assessed in a normocalcemic calf. PTH secretion rate was maintained above the preinfusion level throughout the course of a 3-h iv infusion. A large portion of the immunoreactivity in parathyroid venous plasma, collected from two hypocalcemic calves during and before epinephrine infusion, eluted from the gel column coincident with radioiodinated purified bovine PTH. However, a lesser amount of the immunoreactivity that was recognized only by the carboxyl- terminus-specific RIA eluted from the gel column after the radiolabeled PTH. These results indicate that the immunoreactivity was comprised not only of intact PTH (84 aminoacids) but of a biologically inactive hormonal fragment as well. The proportion of the two forms of immunoreactivity was not changed by epinephrine administration. Since apparently physiological quantities of epinephrine are capable of stimulating the secretion of biologically active intact PTH for an extended period of time, we conclude that epinephrine has the potential to participate in the regulation of PTH secretion rate and plasma calcium concentration.