The effect of parasympathetic postganglionic denervation on parotid salivary protein secretion in anaesthetized sheep.
Effects of unilateral parasympathetic denervation of ovine parotid glands were examined in anaesthetized sheep 21-28 days after nerve section. Parasympathetic denervation reduced the mass of the ipsilateral gland while increasing that of the contralateral gland to the extent that total gland mass was greater than in sheep with normally innervated glands. The spontaneous secretion (8.8 +/- 1.1 microl min(-1) g gland(-1)) was significantly less from denervated than from innervated glands of normal control animals (26.0 +/- 2.7 microl min(-1) g gland(-1); P< 0.01) and contained more protein. Rates of flow, and the outputs of sodium and potassium, in response to sympathetic stimulation, were similar from normally innervated and chronically denervated glands, when allowance was made for the discrepancy in weights, whereas the output of protein was significantly enhanced following parasympathetic denervation (innervated--31.4 +/- 7.3 microg g gland(-1), denervated--83.4 +/- 26.6 microg g gland(-1); P< 0.05). Intra-arterial infusions of acetylcholine (130 pmol min(-1) kg(-1)) elicited a flow of parotid saliva, the protein content of which was significantly enhanced by prior parasympathetic denervation. Intra-arterial infusions of vasoactive intestinal peptide (VIP; 2.5 pmol min(-1) kg(-1)) produced a small but statistically significant (P< 0.05) increase in the flow of parotid saliva from the contralateral, innervated but not from denervated glands. It also caused a small increase in protein output, which was significantly enhanced by prior denervation. VIP had no synergistic effect on the parotid responses to acetylcholine. The results show that the parasympathetic innervation to the parotid gland of the sheep exerts important trophic effects on the gland. Interaction of adrenergic and cholinergic receptors makes an important contribution to stimulation of the secretion of protein and prior denervation potentiates the protein responses to both acetylcholine and VIP.
Edwards
A V
AV
Physiological Laboratory, University of Cambridge, UK. ave1000@cam.ac.uk
Titchen
D A
DA
D000109:Acetylcholine / Q000494:pharmacology; D000758:Anesthesia; D000818:Animals; D000831:Animals, Newborn; D001285:Atropine / Q000494:pharmacology; D015740:Calcitonin Gene-Related Peptide / Q000494:pharmacology; D004347:Drug Interactions; D004558:Electric Stimulation; D007261:Infusions, Intra-Arterial / Q000379:methods; D017764:Parasympathectomy / Q000379:methods*; D010275:Parasympathetic Nervous System / Q000502:physiology* / Q000601:surgery; D010276:Parasympatholytics / Q000494:pharmacology; D010306:Parotid Gland / Q000187:drug effects / Q000294:innervation / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D011506:Proteins / Q000187:drug effects / Q000378:metabolism*; D027544:Salvia / Q000187:drug effects / Q000378:metabolism; D012756:Sheep; D012964:Sodium / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000502:physiology; D013997:Time Factors; D014660:Vasoactive Intestinal Peptide / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
D010276:Parasympatholytics; D011506:Proteins; D014665:Vasodilator Agents; D014660:Vasoactive Intestinal Peptide; D001285:Atropine; D012964:Sodium; D015740:Calcitonin Gene-Related Peptide; D000109:Acetylcholine; D011188:Potassium