title: Isoproterenol opens K+(ATP) channels via a beta2-adrenoceptor-linked mechanism in Sertoli cells from immature rats.
abstract: In the present study, we investigated the mechanism by which isoproterenol hyperpolarises membrane potential (MP) in Sertoli cells from seminiferous tubules of 15-day-old rat testes. Modification of MP and resistance (R0) was analysed using conventional intracellular glass microelectrodes. Isoproterenol (2 x 10(-6) M) induced an immediate and significant hyperpolarisation in the Sertoli-cell membrane. The beta2-AR antagonist, butoxamine (1 x 10(-6) M), nullified isoproterenol action. The effect of the beta1 antagonist, metoprolol (1 x 10(-6) M), was light and non-significant. Sulphonylurea glibenclamide inhibition of the K+(ATP) channels suppressed isoproterenol action, and testosterone, while depolarising Sertoli-cell MP closing the K+(ATP) channels through the PLC/PIP2 pathway, reduced beta-AR agonist-induced hyperpolarisation. Also, polycations LaCl3 and spermine reversed isoproterenol's hyperpolarisation effect, probably depolarising the membrane potential through ionic interaction neutralising the action of isoproterenol on K+(ATP) channels. Adenylate cyclase agonist forskolin (0.1 microM) rapidly hyperpolarised Sertoli-cell MP, mimicking the isoproterenol effect. These effects indicate that isoproterenol's action on K+(ATP) channel probably involves the known signalling cascade beta-AR/Gs/AC/cAMP/PKA. These results suggest that the isoproterenol-induced hyperpolarisation is mediated by the opening of K+(ATP) channels in Sertoli cells. This beta-adrenergic hyperpolarisation might play a physiological role in the modulation of MP.
authors.affiliation: Departamento de Fisiologia ICBS, UFRGS, Porto Alegre, Brazil.
authors.forename: A P
authors.initials: AP
authors.lastname: Jacobus
authors.forename: D O
authors.initials: DO
authors.lastname: Rodrigues
authors.forename: P F
authors.initials: PF
authors.lastname: Borba
authors.forename: E S
authors.initials: ES
authors.lastname: Loss
authors.forename: G F
authors.initials: GF
authors.lastname: Wassermann
mesh_terms: D018528:ATP-Binding Cassette Transporters / Q000819:agonists*; D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000818:Animals; D005576:Colforsin / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004594:Electrophysiology; D005905:Glyburide / Q000494:pharmacology; D007004:Hypoglycemic Agents / Q000494:pharmacology; D015640:Ion Channel Gating / Q000187:drug effects; D007545:Isoproterenol / Q000494:pharmacology*; D054086:KATP Channels; D007811:Lanthanum / Q000494:pharmacology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D018408:Patch-Clamp Techniques; D024661:Potassium Channels, Inwardly Rectifying / Q000819:agonists*; D051381:Rats; D017208:Rats, Wistar; D018343:Receptors, Adrenergic, beta-2 / Q000187:drug effects*; D012708:Sertoli Cells / Q000187:drug effects / Q000378:metabolism*; D013739:Testosterone / Q000494:pharmacology
chemical_list: D018528:ATP-Binding Cassette Transporters; D000318:Adrenergic beta-Agonists; D007004:Hypoglycemic Agents; D054086:KATP Channels; D024661:Potassium Channels, Inwardly Rectifying; D018343:Receptors, Adrenergic, beta-2; C092520:uK-ATP-1 potassium channel; D005576:Colforsin; D013739:Testosterone; D007811:Lanthanum; D007545:Isoproterenol; D005905:Glyburide