The salivary flow elicited by phenylephrine was reduced in kininogen-d
eficient rats or by pretreatment of normal Wistar rats with HOE 140, a
bradykinin antagonist. Salivary flow induced by substance P was simil
ar in normal and kininogen-deficient rats. Phenylephrine released larg
e amounts of kallirein in saliva. Isoproterenol was less active while
pilocarpine and substance P induced a small secretion of kallikrein. T
he saliva produced by anaesthetized rats in response to heat stress co
ntained low levels of kallikrein. However a large depletion of the kal
likrein content of submaxillary glands was observed in awake animals e
xposed to 36-degrees-C and 40-degrees-C for one hour. This depletion w
as suppressed by prazosin administered with a beta-adrenergic antagoni
st. Administered alone, these drugs had no effect, whereas atropine in
creased the depletion. The presence of kallikrein was observed in the
oedema fluid which developed around the submaxillary glands in rats pr
etreated with atropine or exposed to 40-degrees-C. A consumption of pl
asma kininogens occured during heat exposure. The reflex-induced relea
se of kallikrein during heat exposure is mainly controled by sympathet
ic nerves through activation of both alpha and beta-adrenoreceptors. T
his release induces the formation of kinins which participate to the t
hermolytic salivation.