Role of Calcium Uptake and Cyclic AMP in the Vascular Effects of PTH

Abstract

There is experimental evidence for a cardiovascular effect of parathyroid hormone (PTH). A rapid positive inotropic and chronotropic action of PTH has been described in different animal species in both in vivo and in vitro conditions (Lhoste et al., 1980; Bogin et al., 1981; Hashimoto et al., 1981; Katoh et al., 1984). Evidence has also been accumulated showing that PTH is hypotensive and is a vasodilator (Charbon, 1968; Charbon and Hustaert, 1974; Schleiffer et al., 1979; Pang et al., 1980; Ellison and Mc Carrón, 1984; Saglikes et al., 1985). These latter effects seem to be a direct relaxation of vascular smooth muscle (Suzuki et al., 1983; Pang et al., 1984; Nickols et al., 1987). The mechanisms responsible for this effect have not been clearly defined although recent reports have described a stimulation of vascular adenylate cyclase activity (Huang et al., 1983; Helwig et al., 1984; Pang et al., 1985; Nickols et al., 1986; Nickols and Cline, 1987; Bergmann et al., 1987). It is generally accepted that cyclic adenosine monophosphate (cAMP) as well as the cytosolic Ca⁺⁺ concentration modulate vascular smooth muscle tone. To gain more information on the mechanisms of vascular effect of PTH we have studied the effects of PTH on contractile responses, transmembrane Ca⁺⁺ fluxes and cAMP content in rat vascular preparations.