Vascular protein leakage in the rat parotid gland elicited by reflex stimulation, parasympathetic nerve stimulation and administration of neuropeptides.

Evans blue accumulated in parotid glands of conscious rats in response to feeding (over 60 min), in the absence of atropine and adrenoceptor antagonists and in their presence, and after pretreatment with the sensory neurotoxin capsaicin. Stimulation of the auriculo-temporal nerve (40 Hz, 10 or 20 min), without and with the blockers, caused Evans blue to accumulate. A periglandular oedema also contained the dye. Administration (i.v.) of neurokinin A accumulated Evans blue, while substance P, vasoactive intestinal peptide (VIP), pituitary adenylate cyclase-activating peptide (PACAP), calcitonin gene-related peptide (CGRP) and pilocarpine lacked effect. Pilocarpine enhanced the action of neurokinin A and, furthermore, substance P combined with either VIP, PACAP or CGRP resulted in accumulation of Evans blue. In the sublingual + submandibular glands, Evans blue increased in response to neurokinin A and pilocarpine; furthermore, substance P and VIP, and substance P and CGRP, interacted positively. Bradykinin lacked effect in the glands. Comparisons were made with the urinary bladder. Accumulation of Evans blue reflects plasma protein extravasation. In salivary glands, the phenomenon occurred during feeding and was independent on intact sensory innervation; instead, the parasympathetic innervation containing the neuropeptides was in focus. In the clinic, the present findings may have implications for the aetiology of gland swelling and pain.