Abstract
The salivary flow elicited by phenylephrine was reduced in kininogen-deficient rats or by pretreatment of normal Wistar rats with HOE 140, a bradykinin antagonist. Salivary flow induced by substance P was similar in normal and kininogen-deficient rats. Phenylephrine released large amounts of kallikrein in saliva. Isoproterenol was less active while pilocarpine and substance P induced a small secretion of kallikrein. The saliva produced by anaesthetized rats in response to heat stress contained low levels of kallikrein. However a large depletion of the kallikrein content of submaxillary glands was observed in awake animals exposed to 36 degrees C and 40 degrees C for one hour. This depletion was suppressed by prazosin administered with a beta-adrenergic antagonist. Administered alone, these drugs had no effect, whereas atropine increased the depletion. The presence of kallikrein was observed in the oedema fluid which developed around the submaxillary glands in rats pretreated with atropine or exposed to 40 degrees C. A consumption of plasma kininogens occurred during heat exposure. The reflex-induced release of kallikrein during heat exposure is mainly controlled by sympathetic nerves through activation of both alpha and beta-adrenoreceptors. This release induces the formation of kinins which participate to the thermolytic salivation.
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