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Centrally Administered Parathyroid Hormone (PTH)-Related Protein(1–34) But Not PTH(1–34) Stimulates Arginine-Vasopressin Secretion and Its Messenger Ribonucleic Acid Expression in Supraoptic Nucleus of the Conscious Rats

First Department of Internal Medicine (S.Y., I.M., K.Z., S.E.) and Physiology (Y.U., H.Y.), School of Medicine, University of Occupational and Environmental Health, 1–1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807, Japan; and Department of Physiology (H.K.), Miyazaki Medical College, 5200 Kihara Kiyotake Miyazaki-gun, Miyazaki, 889–16, Japan

Address all correspondence and requests for reprints to: Isao Morimoto, First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, 1–1 Iseigaoka, Yahatanishi-ku, Kitakyushu, 807, Japan. E-mail: isaomo{at}med.uoeh-u.ac.jp

It has been suggested that PTH-related protein (PTHrP) is an endogenous modulator of cardiovascular systems. We have reported that PTHrP(1–34), but not PTH(1–34), causes the release of arginine-vasopressin (AVP) from the supraoptic nucleus (SON) of the hypothalamus in vitro through a novel receptor distinct from the PTH/PTHrP receptors (type I or type II) described previously. In this study, we have investigated the in vivo effects of PTHrP(1–34) on AVP secretion and its messenger RNA (mRNA) expression in the SON in conscious rats. Intracerebroventricular (icv) administration of PTHrP(1–34) resulted in an increase in plasma AVP concentration in a dose-dependent manner (0–400 pmol/rat). The maximal effect was obtained at 15 min after icv administration of PTHrP(1–34). Neither PTHrP(7–34) nor PTH(1–34) had any effect on plasma AVP levels. PTHrP(1–34)-induced AVP secretion was antagonized by pretreatment with PTHrP(7–34) but not by that with PTH(1–34). In addition, in situ hybridization study revealed that AVP mRNA expression in the SON and paraventricular nucleus was significantly increased 30 min after icv administration of PTHrP(1–34) and reached a maximum at 180 min. Furthermore, in Northern blot analyses, AVP mRNA expression in the SON was increased to approximately a 2-fold of basal level by PTHrP(1–34). On the other hand, neither PTHrP(7–34) or PTH(1–34) had any effect on the mRNA expression. The PTHrP(1–34)-stimulated AVP mRNA expression was eliminated by pretreatment with PTHrP(7–34) but not with PTH(1–34). These results suggest that, in the central nervous system, PTHrP(1–34) is involved in AVP secretion through a novel receptor distinct from the PTH/PTHrP receptors reported previously, playing a role in the body water and electrolyte homeostasis.

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