Bradykinin and functional vasodilatation in the salivary gland

Abstract

Blood flow through the submandibular gland of the dog was measured and the venous effluent monitored for potential mediators of the functional vasodilatation by passing it over a series of assay tissues. On chorda lingual nerve stimulation there was salivation, an increased blood flow and the release of a bradykinin-like substance (kinin) into the venous effluent. In about half of the preparations, increasing the frequency of stimulation from 2 to 10 Hz led to an increased output of kinin, whereas in the others successive stimulations led to a decreasing output of kinin in the face of normal secretory and vascular responses. Following the administration of atropine, the vasodilatation persisted, salivation was abolished and after several stimulations kinin release could no longer be detected. Release of prostaglandin did not appear to be responsible for the vasodilatation. It is concluded that neither kallikrein nor kinin is the main mediator of parasympathetic vasodilatation in the salivary gland.