Abstract

Parathyroid hormone (PTH) has been demonstrated to be an important hormone in the maintenance of calcium and phosphate homeostasis in the vertebrate body. It keeps the plasma calcium and phosphate levels within a narrow range by regulating bone, intestinal and renal handling of these electrolytes. Many recent reports have described some “new” actions of PTH in target tissues, including a variety of smooth muscles, hepatic, adipose and juxtaglomerular (JG) cells. The effects on vascular smooth muscle tissue have probably been the most extensively investigated. However, the vascular or hypotensive action is, in fact, not so “new” as one thinks. It is as “old” as the discovery of PTH itself. When Collip and Clark (1925) first extracted PTH from the parathyroid glands, it was tested on dog blood pressure and a hypotensive effect was reported. Since then, there have been a number of reports on the vasodilating action of PTH extracts or synthetic fragments containing the amino terminal 1–34 [PTH-(l–34)] (Handler & Cohn, 1952; Charbon, 1966; Charbon & Hulstaert, 1974; Berthelot & Gairard, 1975; Nickols et a7., 1986). There is, however, considerable scepticism about these new actions of PTH because the concentration of PTH needed to produce such effects often exceeds that reasonably expected to be found in the circulation. The physiological meaning of such pharmacological actions therefore remains doubtful. Nevertheless, many of these actions are probably receptor mediated.

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