The rate of flow and electrolyte concentration of parotid saliva were measured before, during and after intravenous and contralateral intracarotid infusion of KCl (0.5 mol.1(-1)) and NaCl (0.5 mol.1(-1)) at 385-625 mumol. min(-1) for 40 min into 5 sheep. In intact conscious sheep contralateral intracarotid infusion of KCl caused marked depression of salivary secretion in all experiments whereas infusion of NaCl had no consistent effect on flow. Intravenous infusion of KCl 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 KCl either had no effect on flow or caused an increase in flow. After ipsilateral cervical sympathectomy contralateral intracarotid infusion of KCl 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 KCl 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 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.

Salivary flow rate and the concentrations of electrolytes in parotid saliva and arterial plasma from anaesthetized sodium-replete sheep were measured before, during and after ipsilateral intracarotid infusion of acetylcholine at 10 nmol min -1 to ascertain whether anaesthesia altered the relation between salivary flow and sodium concentration. The potential difference (PO) between the lumen of the parotid duct and the vascular system was also measured. Concentrations of salivary sodium and phosphate were decreased and potassium concentration and total CO2 content were increased when rate of salivary flow was increased by acetylcholine infusion. Salivary chloride concentration was reduced in five experiments and increased in three experiments when flow rate was elevated. Thus the flow-composition relations of parotid saliva from anaesthetized sheep were essentially the same as those for saliva from conscious animals. The PO between the lumen of the parotid duct and blood at resting flow rates was 9·4± 1·07 mY, lumen negative. At high flow rates, stimulated by acetylcholine infusion, the PO increased to 21· 9 ± 2· 20 mY, lumen negative. This increase in PO of the duct epithelium appeared to depend on changes in the composition of saliva arriving at the site of potential measurement.

Saliva was collected from the parotid salivary gland of anaesthetized sodium-replete red kangaroos (Macropus rufus) by catheterization of the parotid duct through its opening in the mouth. Salivary secretion was stimulated by ipsilateral intracarotid infusion of acetylcholine at varying rates to produce salivary flow rates ranging from 0.056 +/− 0.0042 (S.E. of mean) to 4.509 +/− 0.1136 ml min-1. The concentrations of sodium (142.2 +/− 1.93 to 157.0 +/− 1.17 mmol l-1), calcium (40.1 +/− 7.08 to 72.8 +/− 8.0 mumol l-1) and bicarbonate (68.6 +/− 3.48 to 143.3 +/− 0.67 mmol l-1) and the osmolality (270.1 +/− 2.98 to 291.7 +/− 2.10 mosmol kg-1) were positively correlated with salivary flow rate, whereas the concentrations of potassium (11.4 +/− 0.57 to 6.92 +/− 0.19 mmol l-1), magnesium (206.0 +/− 34.1 to 9.3 +/− 0.78 mumol l-1), hydrogen ion (17.0 +/− 1.89 to 6.82 +/− 0.49 nmol l-1), chloride (30.7 +/− 2.41 to 4.11 +/− 0.23 mmol l-1) and phosphate (47.6 +/− 2.65 to 14.9 +/− 0.81 mmol l-1) were negatively correlated with flow rate. The relationships between flow rate and concentration were curvilinear for all the inorganic solutes. The rates of secretion for each ion and for total solute were positively correlated with salivary flow rate. These regressions for sodium, potassium, calcium, hydrogen ion, bicarbonate and osmolality were always linear, with highly significant correlation coefficients and variance ratios, which indicated that the changes in concentration of these ions were related solely to flow rate and were not due to any other factor modifying glandular function. Spontaneous secretion was not observed during anaesthesia.

Intracarotid infusions of noradrenaline (0.3 nmol.kg(-1) x min(-1)) stimulated salivary fluid secretion and caused increases in salivary concentrations of protein, potassium. magnesium. chloride and phosphate, and decreases in bicarbonate. These effects of intracarotid noradrenaline were not reduced by simultaneous intracarotid infusion of phentolamine (3.0 nmol.kg(-1) x min(-1)) but were significantly greater than the responses accompanying intravenous noradrenaline infusion. Concomitant administration of the beta-antagonist, CGP20712A, were much more effective in blocking the noradrenaline-induced changes in salivary composition than equimolar infusions of the beta2-antagonist, ICI118551, thereby confirming the presence of beta1-adrenoreceptors. Intracarotid infusion of salbutamol at 0.6 nmol x kg(-1) x min(-1) and 6.0 nmol x kg(-1) x min(-1) caused increasing but qualitatively similar changes in salivary composition to intracarotid noradrenaline but was less effective than noradrenaline in augmenting salivary protein release. Equimolar intravenous infusions of salbutamol and noradrenaline were equally potent in altering salivary electrolyte concentrations but salbutamol by this route had less effect on protein release and fluid secretion. Concurrent intravenous and intracarotid infusions of beta1-(CGP) and beta2-(ICI) antagonists with intracarotid salbutamol showed that the beta2-antagonist was more potent than the beta1-antagonist by the intracarotid route thereby demonstrating the presence of glandular beta2-receptors and eliminating the possibility that the response to salbutamol was due totally by reflex increases in general sympathetic tone triggered by lowered blood pressure. It was concluded that the kangaroo parotid has functional beta1- and beta2-adrenoreceptor subtypes in endpieces whereas the data provide little support for either adrenoreceptor subtype being present in the excurrent duct system.

Intracarotid infusions of l-phenylephrine at 1.0 nmol.kg(-1).min(-1) or(.)10 nmol.kg(-1).min(-1) were accompanied by increases in salivary protein, urea, magnesium and bicarbonate, and by decreases in osmolality, hydrogen ion activity, sodium, potassium and chloride relative to cholinergically stimulated saliva. Intravenous infusions of phenylephrine at the same dose rates had much less effect on salivary composition with the differences between the routes of administration being greatest for the higher dose rate. Propranolol administered with phenylephrine via the carotid artery, at an antagonist:agonist ratio of 10:1, was much more effective in blocking the phenylephrine-induced changes in salivary composition than equimolar infusion of phentolamine with phenylephrine. Simultaneous intracarotid infusions of either a beta(1)-antagonist (CGP20712A) or a beta(2)-antagonist (ICI118551) with phenylephrine showed that ICI118551 was more potent than CGP20712A at preventing the changes in salivary composition associated with phenylephrine administration. It was concluded that alpha(1)-adrenoreceptors were not present in functionally significant numbers in the gland and that the effect of phenylephrine on the kangaroo mandibular was mediated by beta-adrenoreceptors predominantly of the beta(2)-subtype. As the phenylephrine dose rates in the kangaroos were comparable with those used to determine alpha-adrenergic responses of eutherian salivary glands and as both propranolol and phentolamine appeared to have minor beta-sympathomimetic activity, at least one subtype of beta-adrenoreceptors in macropods may not be identical to its eutherian counterpart.