Premium
THE RôLE OF THE AUTONOMIC NERVOUS SYSTEM IN THE DEPRESSION OF PAROTID SALIVARY SECRETION DURING HYPERKALAEMIA IN CONSCIOUS SHEEP
Author(s) -
Beal A. M.
Publication year - 1977
Publication title -
quarterly journal of experimental physiology and cognate medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0033-5541
DOI - 10.1113/expphysiol.1977.sp002403
Subject(s) - autonomic nervous system , depression (economics) , medicine , neuroscience , psychology , cardiology , heart rate , economics , macroeconomics , blood pressure
The rate of flow and electrolyte concentration of parotid saliva were measured before, during and after intravenous and contralateral intracarotid infusion of KC1 (0·5 mol.1 ‐1 ) and NaCl (0·5 mol.1 ‐1 ) at 385–625 µmol. min ‐1 for 40 min into 5 sheep. In intact conscious sheep contralateral intracarotid infusion of KC1 caused marked depression of salivary secretion in all experiments whereas infusion of NaC1 had no consistent effect on flow. Intravenous infusion of KC1 into the intact conscious sheep caused a slight depression of salivary secretion but minimum flow was significantly higher than that during intracarotid infusion. When the sheep were anaesthetized salivary flow rates were low and contralateral intracarotid infusion of KC1 either had no effect on flow or caused an increase in flow. After ipsilateral cervical sympathectomy contralateral intracarotid infusion of KC1 into the conscious sheep caused a marked depression of salivary flow similar to that occurring when the sheep were intact. After section of the secretomotor nerve of the gland salivary flow rates were low and contralateral intracarotid infusion of KC1 had no effect on flow. The salivary flow responses of the sheep were consistent, regardless of whether the KC1 infusions were given within 24 h or 1—2 weeks after cervical sympathectomy or secretomotor nerve section. Salivary sodium concentration was negatively correlated with salivary flow in all experiments. It was concluded that potassium acted at a site located in the head but not by direct action on the salivary gland. The depression of salivary secretion by hyperkalaemia resulted from a decline in neural activity in the parasympathetic secretomotor innervation of the parotid gland.