Water stimulation of the posterior oral cavity induces inhibition of gastric motility

The response of gastric motility to the administration of water and saline in the larynx and epiglottis was investigated in urethan-chloralose anesthetized rats. Administration of water inhibited motility of the distal stomach, but 0.15 M NaCl did not induce the inhibitory response. Bilateral sectioning of the superior laryngeal nerve (SLN) abolished the inhibitory response induced by water. Bilateral cervical vagotomies abolished the inhibitory responses, although spinal transection did not affect the inhibitory response. These inhibitory responses have been observed in immobilized animals. The degree of inhibition by water and hypotonic saline was negatively correlated with the sodium concentration. In contrast, the degree of inhibition to hypertonic saline was positively correlated with the sodium concentration. The proximal stomach also showed a reduction in intragastric pressure in response to the administration of water. These findings suggest that water-responsive afferent neurons in the SLN suppress gastric motility via the vagal efferent nerve.

Central somatostatin prevents vagal efferent nerve excitation produced by TRH but not by 2-deoxy-D-glucose

Thyrotropin-releasing hormone (TRH) administered intracerebroventricularly and intravenous injection of 2-deoxy-D-glucose (2-DG) stimulate pancreatic exocrine secretion via vagal efferent nerve excitation. We examined whether centrally administered somatostatin would inhibit pancreatic exocrine secretion that was stimulated by vagal efferent nerve excitation in conscious rats. The animals were prepared with cannulas draining bile and pancreatic juice separately and with a duodenal cannula, a cerebroventricular cannula, and a right jugular vein cannula. Intracerebroventricular injection of somatostatin (0.4 or 4 nmol) significantly inhibited pancreatic secretion induced by TRH (50 or 500 pmol) in a dose-dependent manner. Intravenous injection of somatostatin had no effect on pancreatic secretion stimulated by TRH. On the other hand, somatostatin injected centrally did not affect pancreatic secretion induced by 2-DG (75 mg/kg) or basal secretion. These results suggest that TRH and 2-DG stimulate vagal efferent nerves via distinct mechanisms and that central somatostatin selectively inhibits excitation of the vagus induced by peptidergic (TRH) stimulation.

Regulation of central vascular blood flow in the turtle

The purpose of this study was to determine the effects of vagal nerve stimulation on the pulmonary and systemic circulations in the turtle Pseudemys scripta. The heart rate (HR), systemic vascular resistance (Rsys), pulmonary vascular resistance (Rpul), total pulmonary blood flow (Qpul), and total systemic blood flow (Qsys) were measured during electrical stimulation of the vagal efferent and the vagal afferent nerves. Vagal efferent nerve stimulation resulted in a bradycardia, increased Rsys and Rpul, and a 60% reduction in the Qpul and Qsys. These cardiovascular changes were eliminated after an intravenous injection of atropine. In contrast, vagal afferent nerve stimulation resulted in a tachycardia, a twofold increase in Rsys, a reduction in Rpul, and an 85% increase in Qpul. These changes were eliminated after pretreating the animals with bretylium tosylate (10 mg/kg). An intravenous infusion of epinephrine (0.1 micrograms/kg) produced cardiovascular changes similar to vagal afferent stimulation. The cardiovascular changes resulting from afferent and efferent nerve stimulation were similar to the cardiovascular adjustments often associated with intermittent lung ventilation in reptiles. The results of our study suggest that such cardiovascular changes are under cholinergic and adrenergic control.

Role of nitric oxide in esophageal peristalsis

In vitro studies have suggested that NO may be a nonadrenergic, noncholinergic inhibitory mediator in the esophageal body. We examined the role of NO in physiological peristalsis in anesthetized opossums by assessing the effect of the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) on esophageal contractions induced by swallows, prolonged vagal efferent nerve stimulation, and midesophageal balloon distension. A perfused manometry system measured intraluminal pressures 1 and 5 cm orad to the lower esophagus, and suction electrodes monitored membrane potential changes at the same locations. NO synthase inhibition 1) decreased swallow-induced contraction amplitude in the distal esophagus and, when combined with atropine, abolished these contractions; 2) diminished swallow-induced contraction latencies, predominantly in the distal esophagus, thereby decreasing the latency gradient and increasing the peristaltic velocity; 3) abolished vagal-stimulation-induced, end-of-stimulus “B” contractions and either unmasked or increased the amplitude of intrastimulus “A” contractions; 4) abolished the contractions occurring at the end of balloon distension; and 5) inhibited the membrane hyperpolarization and the subsequent nonadrenergic, noncholinergic depolarization induced by all three stimuli. These data support the hypothesis that NO is a mediator of nonadrenergic, noncholinergic neurotransmission in the opossum esophagus. Furthermore, the data suggest that esophageal peristalsis is mediated by a “blended” activation of cholinergic and nonadrenergic, noncholinergic (via NO) neurons