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Ranakinin, a Naturally Occurring Tachykinin, Stimulates Phospholipase C Activity in the Frog Adrenal Gland¹

European Institute for Peptide Research (IFRMP no. 23), Laboratory of Cellular and Molecular Neuroendocrinology, INSERM U-413, UA CNRS, University of Rouen (M.K.K., L.D., M.-C.T., H.V.), 76821 Mont-Saint-Aignan, France; the Department of Animal Biology, University of Torino (L.L., A.F.), 10123 Torino, Italy; and the Regulatory Peptide Center, Department of Biomedical Science, Creighton University Medical School (J.M.C.), Omaha, Nebraska 68178

Address all correspondence and requests for reprints to: Dr. H. Vaudry, European Institute for Peptide Research (IFRMP n°23), Laboratory of Cellular and Molecular Neuroendocrinology, INSERM U413, UA CNRS, University of Rouen, 76821 Mont-Saint-Aignan, France. E-mail: hubert.vaudry{at}univ-rouen.fr

We have previously shown that the frog adrenal gland is innervated by a dense network of fibers containing ranakinin, one of the endogenous tachykinins in the amphibian Rana ridibunda, and we have found that ranakinin stimulates in vitro corticosteroid secretion by frog adrenal tissue. To elucidate the mechanism of action of ranakinin on the frog adrenal gland, we investigated the effect of ranakinin on cAMP formation and polyphosphoinositide metabolism. Incubation of frog adrenal explants with various tachykinins, including ranakinin, substance P, neurokinin A, or neurokinin B, did not produce any significant modification of cAMP concentrations. In contrast, ranakinin induced a time- and dose-dependent stimulation of inositol phosphate formation with a concomitant decrease in membrane polyphosphoinositides. Pretreatment of the tissue slices with the phospholipase C inhibitor U-73122 or with pertussis toxin completely abolished the stimulatory effect of ranakinin on inositol phosphate formation. Prolonged administration of U-73122 to perifused frog adrenal explants markedly attenuated the ranakinin-evoked stimulation of corticosterone and aldosterone secretion. Taken together, these data indicate that in the frog adrenal gland, ranakinin has no effect on the adenylyl cyclase system, but enhances polyphosphoinositide hydrolysis. The stimulatory action of ranakinin on inositol phosphate formation and corticosteroid secretion is mediated through activation of a phospholipase C positively coupled to a pertussis toxin-sensitive G protein.