Search

1. Intra-arterial infusions of vasoactive intestinal polypeptide (VIP) were made in anaesthetized lambs in which activity of the reticulo-omasal orifice (ROO) was recorded manometrically and in conscious lambs in which activity of the reticulum, ROO and abomasum were recorded by electromyographic (EMG) techniques. 2. Spontaneous rhythmic opening and closing movements of the ROO occurred in anaesthetized lambs at 3-5 min-1. Infusions of VIP into the left gastric artery at rates of 0.5-3.0 nmol min-1 produced changes in activity of the ROO. Within 120 s of commencement of the infusions there was an increase in frequency and magnitude of the movements of the ROO for up to 120 s. This was followed with infusion of VIP at the lower levels (0.5-1.0 nmol min-1), by a marked reduction and sometimes complete loss of the rhythmic movements. There was always complete cessation of activity of the ROO with infusion of VIP at 1.5-3.0 nmol min-1. 3. In conscious lambs the frequency of the diphasic reticular EMG bursts which recur at intervals of ca. 1 min was not affected by infusions of VIP at 3.0 nmol min-1 for 10 min. 4. Between each diphasic reticular EMG burst in the conscious lamb there was normally phasic activity of the ROO consisting of EMG bursts of long (ca. 4 s) and short (ca. 1 s) duration. Within 90 s of commencement of infusion of VIP at 3.0 nmol min-1 short-burst EMG activity disappeared with the remaining long bursts being of greater duration (5.4 +/- 1.2 s) than before infusion. After a series of four to fifteen such more prolonged long bursts there was quiescence of the EMG of the ROO. After infusion of VIP EMG activity recommenced first as a series of eight to fourteen long bursts which was followed by the reappearance also of short-burst activity. Infusions of VIP at 8-10 nmol min-1 produced a more prompt cessation of EMG activity of the ROO. Of other peptides which were infused only PHI (a peptide with N-terminal histidine and C-terminal isoleucine amide) produced cessation of the EMG activity of the ROO. However, on a molar basis VIP was 2-3 times more potent than PHI in causing cessation of activity of the ROO. 5. Infusion of VIP at 3.0 nmol min-1 produced a cessation or diminution of EMG activity of the body, antrum and pylorus of the abomasum.(ABSTRACT TRUNCATED AT 400 WORDS)

1. Effects of the vagus nerves on the activity of the reticulo-omasal orifice (ROO) and the abomasum and the concentration of vasoactive intestinal polypeptide (VIP) in gastric and intestinal venous effluent were studied in anaesthetized lambs. 2. Both excitatory and inhibitory effects of the vagus on the ROO and abomasum were demonstrated. Excitation of activity of the ROO was dominant with stimulation at lower frequencies (less than or equal to 20 Hz) whereas higher frequencies (50-70 Hz) caused inhibition. 3. Inhibition but not stimulation of the ROO and abomasum were obtained with vagal stimulation after administration of atropine (200-500 micrograms kg-1 I.V.). 4. The concentration of VIP in gastric venous effluent blood rose by 41 +/- 10 pmol l-1 (n = 13) within 90 s of the start of stimulation (10 Hz, 5 ms pulse duration, 10 V for 180 s) of a vagus nerve and fell within 60 s of its cessation to or near basal levels. The effects of vagal stimulation in changing the concentration of VIP were not altered by administration of atropine. 5. The concentration of VIP in the intestinal venous effluent increased during stimulation (10 Hz, 5 ms pulse duration, 10 V, for 180 s) of a vagus nerve by 15 +/- 5 pmol l-1 (n = 11) and remained elevated for more than 10 min after the stimulus had ceased. 6. The changes in gastric motility and in concentration of VIP in gastric and intestinal venous blood with stimulation of the vagus nerves have been discussed in relation to similar alterations which occur in lambs during sucking of milk.

Vasoactive intestinal polypeptide (VIP) has been proposed as the neurotransmitter of the atropine-resistant relaxation of gastric structures in the lamb. To examine this proposal VIP concentrations in plasma from arterial, gastric venous and intestinal venous blood were measured in healthy conscious lambs before, during and after teasing with, and sucking of milk. Basal arterial plasma VIP concentrations were undetectable (less than 3 pmol/l) and remained so during and after feeding. Before feeding VIP was detected in only 2 of 12 gastric venous plasma samples (5 and 13 pmol/l). During teasing with food there were increments in VIP of 19 +/- 4 pmol/l and during feeding of 27 +/- 5 pmol/l. VIP concentration in gastric venous plasma rapidly returned to fasting levels after cessation of sucking. In contrast VIP in the intestinal venous plasma did not rise during teasing or upon commencement of sucking but a peak increment of 34 +/- 6 pmol/l occurred at 5 min after cessation of feeding. The results are consistent with the hypotheses that VIP is released in anticipation of and during sucking from inhibitory neurones involved in relaxation of gastric structures and that intestinal release of VIP is a consequence of entry of digesta into the small intestine.

The effects, on secretion of fluid and protein from the submaxillary gland of intracarotid injections of acetylcholine or vasoactive intestinal polypeptide (VIP), and intracarotid infusions of VIP during a background of muscarinic stimulation, were examined in sheep and pigs. Intracarotid injections of VIP produced secretion of saliva from the ovine gland which continued after administration of atropine, phentolamine and propranolol. The protein concentration of this saliva was over 5-fold greater than that secreted in response to acetylcholine. Intracarotid injection of VIP did not evoke secretion from the porcine submaxillary gland but increased 3-fold the protein concentration in saliva evoked by subsequent intracarotid injection of acetylcholine. Intracarotid infusions of VIP in sheep produced dose-related increases in both flow (up to 1.9-fold) and protein concentration (up to 42-fold) of submaxillary saliva secreted in response to a background infusion of bethanechol. In pigs, intracarotid infusions of VIP at 0.015, 0.15 and 1.5 nmol/min produced increases in both flow and protein concentration of bethanechol-evoked saliva. The increases in protein concentration (up to 2.8-fold) were dose-related, but the increases in flow were not, being ca. 25% with each dose of VIP. The experiments provide evidence that VIP may effect mobilization of protein into saliva even in a species (pig) in which VIP does not evoke secretion of fluid.