Alpha 2-adrenoceptor regulation of parathyroid hormone function in the isolated perfused kidney

We investigated physiological interactions between alpha 2-adrenoceptors and parathyroid hormone (PTH) in the isolated buffer-perfused kidney. PTH infusion (10nM) caused a rapid and significant rise in cAMP excretion which diminished despite continued hormone infusion. PTH also caused a delayed phosphaturia which peaked 20-30 minutes following the start of PTH infusion. alpha 2-Adrenoceptor stimulation with epinephrine (28nM) diminished PTH-stimulated cAMP accumulation by 68-71% (p less than 0.05) but had no effect on PTH-induced phosphaturia. None of the experimental interventions affected renal hemodynamics. In additional studies, we used lithium (1mM) as a marker of proximal tubular sodium transport. PTH caused a rapid rise in lithium excretion which was temporally distinct (maximum response in 0-10 minutes) from the phosphaturia. alpha 2-Adrenoceptor stimulation completely blocked the inhibitory effect of PTH on lithium reabsorption. These results suggest that alpha 2-adrenoceptors regulate the stimulatory effect of PTH at proximal tubular adenylate cyclase. However, alpha 2-adrenoceptors play no role in phosphate transport in this segment. alpha 2-Adrenoceptor stimulation reverses PTH-induced lithium excretion, suggesting physiological antagonism in the proximal tubule, most likely involving Na/H exchange.