Effects of stimulation of the chorda tympani in bursts on submaxillary responses in the cat

Abstract

SUMMARY1. The effects of continuous preganglionic stimulation of the chorda tympani at 2 Hz for 10 min were compared with those of stimulation at 20 Hz in 1 see bursts at 10 see intervals for the same period in cats treated with atropine (0-5 mg/kg). Both the fall in mean submaxillary vascular resistance (s.v.r.) and the rise in mean vasoactive intestinal peptide (VIP) output from the gland were increased significantly (P < 0-01; P < 0 02) when the same total number of impulses were delivered in the form of bursts at the higher frequency.2. Both responses were also consistently increased by stimulating the postganglionic innervation in bursts in atropinized cats, or by stimulating the preganglionic innervation in bursts in the absence of atropine.3. The effects of stimulation of the chorda tympani in 1 see bursts at 10 see intervals for 2-3 min were investigated over the frequency range 2-160 Hz. The change in mean s.v.r. under these conditions was significantly reduced by administration of atropine at frequencies between 2 and 20 Hz, but not at higher frequencies. In atropinized cats, the fall in mean s.v.r. was linearly related to stimulus frequency (r = 0 993) over the range 2-60 Hz and a maximal response was obtained during stimulation at 80 Hz. In the same experiments the fall in mean s.v.r. was linearly related to log mean VIP output over the frequency range 20-160 Hz (r = 0 998).4. Closely similar changes in mean s.v.r occurred in response to both pre-and post-ganglionic stimulation at all frequencies tested between 2 and 160 Hz in atropinized cats when the stimuli were delivered in bursts. The changes in mean s.v.r. were not significantly affected by varying the duration of individual stimuli over the range 0-1-25-0 msec.5. The flow of submaxillary saliva was also linearly related to stimulus frequency over the range 2-40 Hz (r = 0 997) when the stimuli were delivered in bursts in the absence of atropine and secretion of saliva was maximal at 60 Hz.6. It is concluded that release of VIP from the submaxillary gland of the cat is optimal in response to stimulation of the chorda tympani at relatively high frequencies, when the impulses are delivered in bursts. Flow of saliva which is mediated by acetyl choline, may also be potentiated under the same conditions.

Cholinergic and VIPergic vasodilator actions of parasympathetic nerves on the thyroid blood flow in rats.

“…prostaglandins, histamine, kinins, neuropeptides (such as VIP and calcitonin gene related polypeptide (CGRP)). It is known that activation of both VIP-containing and cholinergic parasympathetic nerves can contribute to vasodilation in salivary glands in cats (ANDERSSON et al, 1982). It has been demonstrated immunohistochemically by AHREN et al (1980) that there are VIP-containing nerve fibers in the thyroid glands and that these fibers surround the thyroid blood vessels as well as run between thyroid follicle cells.…”

“…Vasoactive intestinal peptide (VIP), a polypeptide containing 28 amino acid residues, was first isolated from hog upper intestinal tissue by SAID and MUTT (1970). Parasympathetic vasodilatory actions have been intensively studied in the salivary gland of the cat by LUNDBERG et al (1980), EDWARDS (1980), andANDERSSON et al (1982). They reported that salivary blood vessels received both parasympathetic cholinergic and VIPergic vasodilatory fibers.…”

Vitamin D and parotid gland function in the rat.

“…An alternate proposal is that the local hyperaemia of salivation is mediated by kallikreins released directly from secreting salivary glands; the physiological importance of this mechanism, however, has been questioned (Schachter, 1969;Regoli & Barabe, 1980). For example, in a recent study inhibition of the kallikrein-kinin cascade by local arterial infusion of aprotinin had no effect on parasympathetically evoked glandular vasodilatation or salivation in a cat submandibular gland preparation perfused in situ (Andersson, Bloom, Edwards & Jarhult, 1982). Regardless of the precise mechanisms involved, it can be argued that vitamin-D-dependent changes in the response of the heart and/or vascular smooth muscle to agonists such as pilocarpine may account for the changes in parotid function observed in vitamin-D-deficient rats.…”

Effects of Reducing Submandibular Blood Flow on Secretory Responses to Parasympathetic Stimulation in Anaesthetized Cats

“…Alternatively, it could be occurring entirely via the constitutive vesicular route under these conditions (Proctor, 1998) involving no loss of granules at all and with secretion rapidly followed by resynthesis as has been reported to occur in the parotid gland of the rat (Asking & Gj orstrup, 1987). At higher frequencies of C-L stimulation vasoactive intestinal peptide (VIP) is released from the postganglionic nerve terminals in this gland (Andersson et al 1982), which potentiates secretion of protein (Ekstr om & Tobin, 1990) with nitric oxide implicated both pre-and postsynaptically (Buckle et al 1995;Edwards et al 1996). It seems likely that protein would be released by exocytosis under these conditions.…”