title: Vasopressin and angiotensin induce inositol lipid breakdown in rat adenohypophysial cells in primary culture.
abstract: Adenohypophysial cells from female Wistar rats were dispersed and maintained for 4 days in primary culture in the presence of [3H]myoinositol. The effects of several releasing hormones, corticotropin-releasing factor (CRF), arginine vasopressin (AVP), angiotensin II (A II), thyrotropin-releasing hormone (TRH), and luteinizing hormone-releasing hormone (LHRH) on the liberation of labelled inositol phosphate (InsP), inositol-bisphosphate (InsP2), and inositol-trisphosphate (InsP3) from prelabelled inositol lipids were tested alone and in combination. Of the corticotropin (ACTH) secretagogues tested, AVP and A II produced a dose-dependent increase in inositol phosphate accumulation. CRF was inactive. The ED50 values of about 1 nM for both AVP and A II were close to the corresponding dissociation constants for binding to pituitary membranes: and, in the case of A II, close to the ED50 for A II-induced inhibition of pituitary membrane adenylate cyclase. The responses to A II and AVP could be inhibited by [Sar1,Ile8]A II and the AVP antagonist d(Et2)-VAVP, respectively. The magnitude of the maximal effect of AVP on accumulation of inositol phosphates was small (25% increase over basal value) suggesting that this effect was restricted to a minor subpopulation of pituitary cells (probably corticotrophes). CRF did not potentiate AVP-induced inositol phosphates accumulation. Maximal A II-induced increase in inositol phosphates accumulation represented 150% of the basal value and was partially additive with that of TRH suggesting that lactotrophes represent the main A II-sensitive subpopulation.
authors.affiliation: Centre de Pharmacologie-Endocrinologie, Montpellier, France.
authors.forename: G
authors.initials: G
authors.lastname: Guillon
authors.forename: R C
authors.initials: RC
authors.lastname: Gaillard
authors.forename: P
authors.initials: P
authors.lastname: Kehrer
authors.forename: P
authors.initials: P
authors.lastname: Schoenenberg
authors.forename: A F
authors.initials: AF
authors.lastname: Muller
authors.forename: S
authors.initials: S
authors.lastname: Jard
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology*; D002478:Cells, Cultured; D002852:Chromatography, Ion Exchange; D003346:Corticotropin-Releasing Hormone / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005260:Female; D007294:Inositol / Q000378:metabolism*; D007295:Inositol Phosphates / Q000378:metabolism; D008053:Lipid Mobilization; D010903:Pituitary Gland, Anterior / Q000378:metabolism*; D011863:Radioimmunoassay; D051381:Rats; D013973:Thyrotropin-Releasing Hormone / Q000494:pharmacology; D013997:Time Factors
chemical_list: D007295:Inositol Phosphates; D000804:Angiotensin II; D001127:Arginine Vasopressin; D007294:Inositol; D013973:Thyrotropin-Releasing Hormone; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D000242:Cyclic AMP