Renal Adenylate Cyclase Stimulating Action of Normal and Oxidized Parathyroid Hormone (1–34)

Abstract

Parathyroid hormone (PTH) has a number of actions which can be demonstrated in vivo and in vitro assays. It has been shown to be hypercalcemic, hypocalciuric, hypophosphatemic, hyperphosphaturic, renal cortical membrane adenylate cyclase stimulating, renal 1-hydroxylase stimulating, and bone calcium mobilizing (see review by Parsons, 1979). Recently, PTH has also been studied extensively for its action on contraction of various smooth muscles. Although it has been repeatedly reported that PTH is hypotensive or vasodilating (Collip & Clark, 1925; Handler & Cohn, 1952; Charbon, 1966; Charbon & Hulstaert, 1974), recent studies from various laboratories have firmly established the vasorelaxing action of PTH (Berthelot & Gairard, 1975; Schleiffer et al., 1979; Pang et al., 1980a; Pang et al., 1985). In addition, the relaxing effect of PTH has been demonstrated in the uterus (Pang et al., 1981; Shew & Pang, 1984a), vas deferens (Zhang et al., 1985), trachea (Yen et al., 1983) and the gastrointestinal tract (Yang et al., 1981). Such a great variety of PTH actions then lead to the question as to whether the receptors are the same in all these target tissues and whether these actions are mediated by the same molecular structural component of the peptide hormone. Some previous attempts to answer such questions will be summarized below. We have recently begun a series of investigations on the adenylate cyclase stimulating action of PTH in rabbit renal microvessel, and tubule preparations. These data will be discussed here in relation to the question raised above.