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      Mechanisms of sympathetic enhancement and inhibition of parasympathetically induced salivary secretion in anaesthetized dogs.

      British Journal of Pharmacology
      Adrenergic alpha-1 Receptor Antagonists, Adrenergic alpha-2 Receptor Antagonists, Anesthesia, Animals, Blood Pressure, drug effects, Dogs, Electric Stimulation, Female, Male, Parasympathetic Nervous System, physiology, Regional Blood Flow, Salivation, Submandibular Gland, blood supply, secretion, Sympathetic Nervous System

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          Abstract

          1. The effects of superimposed and continuous sympathetic nerve stimulation on submandibular parasympathetic salivation were investigated in anaesthetized dogs. 2. Superimposed sympathetic nerve stimulation (1-2 min) initially enhanced and later inhibited salivary secretion induced by parasympathetic nerve stimulation (2-8 Hz) in glands with uncontrolled blood supply or constant-flow vascular perfusion. Propranolol (0.05 mg kg-1, i.a.) did not affect the diphasic sympathetic action whereas phentolamine (0.1 mg kg-1, i.a.) abolished it. Prazosin (0.025 mg kg-1, i.a.) greatly lessened the initial enhancement while yohimbine (0.025 mg kg-1, i.a.) alleviated the late inhibition. 3. Salivary secretion, induced by parasympathetic nerve stimulation (4 Hz) or acetylcholine infusion (10 micrograms kg-1 min-1, i.a.), was abolished by atropine (0.05 mg kg-1, i.a.), increased by phenylephrine infusion (0.25 microgram kg-1 min-1, i.a.) and depressed by clonidine infusion (0.75 microgram kg-1 min-1, i.a.). Hexamethionium (12.5 mg kg-1, i.a.) abolished the nerve-induced secretion but had no effect on the acetylcholine-induced secretion. 4. Continuous background sympathetic nerve stimulation decreased parasympathetic nerve-induced salivary secretion in glands with uncontrolled blood supply or constant-flow vascular perfusion. 5. These results show that parasympathetic salivation can be modified by the sympathetic system at the postsynaptic level; enhancement is via alpha 1-adrenoceptors whereas inhibition is via alpha 2-adrenoceptors.

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