Effects of some α‐adrenoceptor stimulating and blocking agents on the salivary amylase secretion in the rabbit
- 1 April 1984
- journal article
- research article
- Published by Wiley in Acta Physiologica Scandinavica
- Vol. 120 (4) , 567-577
- https://doi.org/10.1111/j.1748-1716.1984.tb07422.x
Abstract
In rabbits under urethane anaesthesia parotid secretion of fluid and amylase in response to electrical stimulation of the sympathetic and parasympathetic nerves was measured before and after injections of various agents acting on α‐adrenoceptors. Amylase secretion in response to sympathetic nerve stimulation at 0.5 and 1 Hz was markedly reduced by clonidine, 0.5–30 μg/kg, in a dose related manner. The effect was not due to an altered responsiveness of the gland, since isoprenaline still caused a large release of amylase. Phenylephrine, 10 μg/kg, and prazosine, 300 μg/kg, had no effect on the sympathetically evoked amylase secretion. Yohimbine in a dose of 0.5 mg/kg increased the amylase output in response to sympathetic nerve stimulation at 0.5 Hz by 70%, while the response at 1 Hz, which is close to maximum for the gland, was not significantly increased. The fluid and amylase secretion produced by parasympathetic nerve stimulation at 1.5, 5.0 and 10 Hz remained unchanged after clonidine, 1.0–30 μg/kg, or yohimbine 0.5 mg/kg. In rabbits provided with chronic parotid fistulae fluid and amylase secretion were studied after injections of clonidine, 30 μg/kg, and yohimbine, 1 mg/kg. In the conscious animal clonidine reduced not only amylase but also fluid secretion, by around 50 and 30%, respectively, indicating an effect on the activity in both the sympathetic and parasympathetic secretory nerves. Yohimbine increased the output of amylase during feeding, seen as an increased mean output of amylase due to an increased concentration of amylase in the saliva, while fluid secretion remained unchanged. The various experiments suggest that amylase secretion in response to sympathetic activation may be influenced by prejunctional control of transmitter release via α‐2‐adrenoceptors, and that this control may be of physiological significance. Parasympathetically evoked secretion does not seem to be under the influence of a similar control.Keywords
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