Mechanisms of the vascular action of parathyroid hormone

The vasodilatory effect of parathyroid hormone (PTH) has been investigated repeatedly and confirmed over the past few years. The present study correlates the PTH-induced vasodilatory effect with the biochemical changes in cyclic AMP (cAMP) content and Ca++ uptake in the vascular tissue. Synthetic fragment bPTH-(1-34) (1.2 X 10(-7) M) significantly inhibited the contraction of the isolated tail artery of rat induced by KCl (30-80 mM). It also relaxed KCl (40 and 60 mM)-induced contractions in a concentration-dependent manner [2.7 X 10(-9) to 3.7 X 10(-8) M)]. In addition, the concentration-contraction curve of Ca (0.3-3.0 mM) was shifted to the right by PTH in 40 mM KCl Krebs-Henseleit solution. These suggest the blocking effects of PTH on Ca entry. This hypothesis was supported by a study in which PTH inhibited KCl-enhanced 45Ca uptake, an effect similar to that of D600. In the experiment with matched tissue, PTH increased tissue cAMP content whereas KCl did not. These suggest that the vascular actions of PTH may involve both cAMP and Ca entry blocking. It is important to know that PTH was capable of stimulating cAMP content in Ca-free medium, suggesting that the increase in cAMP level by PTH may not be secondary to the change in Ca++ uptake.