Beta-adrenergic receptor mechanisms in rat parotid glands: activation by nerve stimulation and 3-isobutyl-1-methylxanthine.
The technique of electrical field stimulation (e.f.s.) was employed in conjunction with selective pharmacological antagonists to specifically investigate the role of endogenous neurotransmitter(s) in the activation of beta-adrenergic receptor mechanisms in isolated parotid gland segments of the rat. The field-stimulus-induced amylase release due to beta-adrenergic receptor activation was characterized as that persisting in the presence of atropine (10(-5) M) and phentolamine (10(-5) M) and susceptible to blockade by propranolol (5 X 10(-6) M), i.e. combined beta 1- and beta 2-receptor blockade. The selective beta 1-receptor antagonist metoprolol (10(-5) M) was as effective as propranolol in blocking the beta-mediated enzyme release. The selective beta 2-receptor antagonist, H35/25 (10(-5) M) did not significantly affect the field-stimulus-induced amylase release. In the absence of any phosphodiesterase inhibitor the levels of cyclic AMP in the tissues were close to the limit of detection. Field stimulation was however associated with a fourfold increase in cyclic AMP. By comparison isoprenaline (10(-5) M) gave rise to a tenfold increase in cyclic AMP. The changes in cyclic AMP metabolism, in response to both field stimulation and isoprenaline, were greatly enhanced in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). The field-stimulus-induced increase in cyclic AMP was abolished by the beta 1-adrenergic receptor antagonist, metoprolol, but persisted in the presence of the beta 2-adrenergic antagonist, H35/25. IBMX was found to have a potent direct effect on amylase release. IBMX (10(-3) M) also gave rise to a tenfold increase in cyclic AMP. IBMX is then as effective as 10(-5) M-isoprenaline in stimulating both enzyme secretion and cyclic AMP metabolism. The secretory response to IBMX was unaffected by beta-adrenergic blockade by propranolol, was independent of extracellular calcium and did not give rise to 86Rb+ efflux. Importantly, isoprenaline (10(-5) M) failed to evoke any significant increase in amylase release if introduced during sustained superfusion of IBMX, yet it is in such protocols that the greatest changes in cyclic AMP metabolism are seen. The study clearly demonstrates that the beta-adrenergic-receptor-regulated amylase release in response to nerve stimulation is mediated predominantly, if not exclusively, by the beta 1-receptor subtype.(ABSTRACT TRUNCATED AT 400 WORDS)[1]References
- Beta-adrenergic receptor mechanisms in rat parotid glands: activation by nerve stimulation and 3-isobutyl-1-methylxanthine. Fuller, C.M., Gallacher, D.V. J. Physiol. (Lond.) (1984) [Pubmed]
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