Parotid salivary flow and composition during infusion of acetylcholine and atropine into the carotid artery of conscious sodium-replete sheep.
The rate of salivary flow and the concentrations of the major electrolytes in parotid saliva and arterial plasma of conscious sodium-replete sheep were measured during resting salivary secretion and when salivary flow was either increased by intracarotid infusion of acetylcholine at 10-30 nmol. min-1 for 20 min or reduced by intracarotid infusion of atropine at 14 nmol. min-1 for 50 min. During both treatments salivary phosphate concentration was always negatively correlated with salivary flow and salivary bicarbonate concentration was always positively correlated with flow. The chloride concentration of the saliva during the acetylcholine infusion experiments was positively correlated with salivary flow whereas when atropine was infused the chloride concentration was negatively correlated with flow. Acetylcholine infusion caused the potassium concentration of the saliva to increase significantly resulting in a marked increase in the total rate of loss of potassium in the saliva. The salivary potassium concentration fell significantly at the onset of the atropine infusion and then rose progressively so that the potassium concentration was elevated by the end of the infusion. In both treatments the concentrations of sodium and hydrion were negatively correlated with salivary flow rate. The maximum sodium concentration which occurred in the low-flow saliva of the atropine infusion was substantially higher than the concentration that would be achieved by equilibrium with the aqueous phase of arterial plasma. It was concluded that the negative correlation between salivary flow and sodium concentration occurred because the reabsorption of sodium from the saliva by the excurrent duct system was minimal in sodium-replete sheep which would have low levels of mineralocorticoids in the circulation. The inconsistency between this  study and previous reports presumably reflects differences in the criteria used to define the sodium status of the animals.
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001285:Atropine / Q000494:pharmacology*; D002245:Carbon Dioxide / Q000032:analysis; D002339:Carotid Arteries; D002712:Chlorides / Q000032:analysis; D005260:Female; D007269:Injections, Intra-Arterial; D009994:Osmolar Concentration; D010306:Parotid Gland / Q000378:metabolism*; D010710:Phosphates / Q000032:analysis; D011188:Potassium / Q000032:analysis; D012463:Saliva / Q000032:analysis; D012472:Salivation / Q000187:drug effects*; D012756:Sheep / Q000378:metabolism*; D012964:Sodium / Q000032:analysis
D002712:Chlorides; D010710:Phosphates; D002245:Carbon Dioxide; D001285:Atropine; D012964:Sodium; D000109:Acetylcholine; D011188:Potassium