Exocrine and endocrine release of kallikrein after reflex‐induced salivary secretion

Exocrine and endocrine release of rat submandibular gland kallikrein has been shown to be low after parasympathetic and β‐adrenergic stimulation but greatly increased after α‐adrenergic stimulation. In the present study, release of glandular kallikrein was investigated under conditions known to give a reflex‐induced salivary gland response.

Heat stress induced a rich flow of saliva originating in the submandibular glands. Salivary kallikrein secretory rate was higher than after parasympathetic stimulation but lower than after sympathetic stimulation (P < 0.005). Only heat stress increased circulating glandular kallikrein (12.7 ± 0.8 ng ml^‐1 before heat exposure and 53.3 ± 14.1 ng ml^‐1 40 min afterwards, P < 0.005). There were no indications that the endocrine release of kallikrein was due to non‐specific leakage. Atropine abolished heatinduced salivation and endocrine kallikrein secretion, possibly through interference with central pathways (P < 0.05). However, phentolamine did not, which may indicate an as yet unidentified mediator of endogenous kallikrein release. The salivary gland response to acid and ether was comparable to that observed after parasympathetic nerve stimulation and was abolished by atropine (P < 0.005). Stimuli known to influence other salivary gland ductal cells, such as aggression and starvation followed by drinking, also did not increase the plasma concentration of glandular kallikrein. The fact that various conditions which induce salivation did not increase circulating glandular kallikrein, coupled with the fact that kallikrein concentration was the highest in animals that died from heat stress, may suggest that the increase in circulating glandular kallikrein seen after heat stress may be pathological and could contribute to the development of heat shock.