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DOI: 10.1055/s-2005-861414
Isoproterenol Opens K+ ATP Channels via a β2-Adrenoceptor-linked Mechanism in Sertoli Cells from Immature Rats
Publikationsverlauf
Received 4 August 2004
Accepted after revision 3 November 2004
Publikationsdatum:
13. Juni 2005 (online)
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 × 10 - 6 M) induced an immediate and significant hyperpolarisation in the Sertoli-cell membrane. The β2-AR antagonist, butoxamine (1 × 10 -6 M), nullified isoproterenol action. The effect of the β1 antagonist, metoprolol (1×10 - 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 β-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 µM) 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 β-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 β-adrenergic hyperpolarisation might play a physiological role in the modulation of MP.
Key words
Isoproterenol - K+ ATP channels - Sertoli cells - β2-Adrenoceptor - Membrane potential
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G. F. Wassermann
Departamento de Fisiologia ICBS, UFRGS
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