Effects of beta-adrenergic agonists in the parotid gland of the rat--an electrophysiological study.

The effects of some beta-adrenergic agonists were studied in the parotid gland of the rat by electrophysiological techniques. In the unoperated gland, isoprenaline caused depolarizations which were slowly developing, long-lasting and of low amplitude. The same response was seen when noradrenaline was combined with alpha-adrenoceptor blocking drugs. A greater number of cells responded to this combination than to isoprenaline. After either parasympathetic or sympathetic denervation 1-3 weeks in advance, to induce supersensitivity, the number of cells responding to beta-adrenoceptor stimulating drugs was significantly increased. In the latter case the threshold dose required to evoke a response was also significantly lowered. Atropine did not have any effect on the isoprenaline-evoked response. The combined parasympathetic and sympathetic denervation did not further increase the responsiveness. It is concluded that beta-adrenoceptor stimulation in the parotid gland of the rat may cause membrane depolarizations. The response is mediated by beta 1-adrenoceptors. The responsiveness is increased in the denervated gland. Secretory studies have demonstrated a supersensitivity to beta-adrenergic agonists as a result of denervation. On the other hand, beta-adrenoceptor stimulation is believed mainly to activate the adenylate cyclase/cyclic AMP system independent of membrane potential changes. It is thus not known if the present 'supersensitivity' is correlated to the increased secretory response earlier demonstrated in this gland.