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Parathyroid Hormone-Related Peptide-(1–34) [PTHrP- (1–34)] Induces Vasopressin Release from the Rat Supraoptic Nucleus in Vitro through a Novel Receptor Distinct from a Type I or Type II PTH/PTHrP Receptor

First Department of Internal Medicine, Department of Pharmacology (N.Y., F.I.), and First Department of Physiology (H.Y.), School of Medicine, University of Occupational and Environmental Health, Iseigaoka, Yahatanishi-ku, Kitakyushu, Japan

Address all correspondence and requests for reprints to: Dr. Isao Morimoto, First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, 1–1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807, Japan.

PTH and PTH-related peptide (PTHrP) bind to a type I PTH/PTHrP receptor expressed in bone and kidney or a type II receptor in nonclassical target tissue with equal affinity and similar bioactivities. PTHrP is abundant in the central nervous system, but its physiological role remains unknown. Herein, we examined the role of PTHrP-(1–34) on arginine vasopressin (AVP) release from the rat supraoptic nucleus (SON). Application of PTHrP-(1–34) to SON slices caused an increase in AVP release in a concentration-dependent manner. Neither PTHrP-(7–34) nor PTH-(1–34) had any effect on AVP release from the SON. PTHrP-(1–34)-induced AVP release was antagonized by a large excess of PTHrP-(7–34) and by H89, an inhibitor of cAMP-dependent protein kinase (A kinase), but not by PTH-(1–34) or PTH-(13–34). PTHrP-(1–34), but not PTH-(1–34), also dose-dependently increased the levels of cAMP in the SON. ¹²⁵I-Labeled PTHrP-(1–34) bound specifically to crude membranes isolated from the SON. Scatchard analysis showed a single class of binding sites for PTHrP-(1–34) with a K_d of 36.4 nM and a maximum binding capacity of 3.94 pmol/mg protein. No specific binding for ¹²⁵I-labeled PTH-(1–34) was noted. The binding of ¹²⁵I-labeled PTHrP-(1–34) was displaced by unlabeled PTHrP-(1–34) and unlabeled PTHrP-(7–34), but not by unlabeled PTH-(1–34). These findings suggest that PTHrP-(1–34), but not PTH-(1–34), causes the release of AVP from the SON through a novel receptor distinct from type I or II PTH/PTHrP receptors.

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