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The responses of the cardiac sympathetic and vagal afferents to H2O2 were analyzed in cats before and after vagotomy to characterize the interactions between the cardiac afferents in the nucleus tractus solitaricus. The stimulation of the cardiac vagal and cardiac sympathetic afferents elicited opposing cardiovascular reflexes that regulated arterial blood pressure, heart rate and myocardial contractility. Furthermore, an intact cardiac vagal afferent system reduced pressor response to sympathetic afferent stimulation.

The interactions between the parasympathetic and sympathetic nervous system were analyzed during the chemical disruption or surgical ablation of the ventral right atrial ganglionated plexus (RAGP) in dogs. Dogs that were administered with local injections of hexamethonium or lidocaine attenuated brachycardia which was induced by vagal stimulation. On the other hand, surgical ablation of the RAGP eliminated the direct vagal influence of the sino-atrial node.

The functional role of pituitary adenylate cyclase-activating polypeptide (PACAP) in the nucleus raphe obscurus (nROb) was analyzed to characterize the mechanisms that modulate gastric motor function. Injection of varying doses of PACAP-38 in rat nROb, dorsal vagal complex and nucleus ambiguus increased peak intragastric pressure in a concentration-dependent manner. However, the effects of PACAP-38 injections were attenuated by bilateral vagotomy indicating the role of PACP in the nROb and vagal complex in mediating gastric motor excitation.

The role of substance P (SP) in the dorsal vagal complex (DVC) on the modulation thyrotropin-releasing hormone (TRH) was analyzed during DVC-induced stimulation of gastric acid secretion in rats. Basal gastric secretion (GAS) response to a TRH analog was reduced in urethan-anesthetized rats by unilateral injections of the stable SP agonists, DiMe-C7, and RX77368. On the other hand, basal GAS was enhanced by the bilateral injection of an SP neurokinin receptor antagonist in rats.

The interaction between glutamate release in the parabrachial nucleus (PBN) of the pons and cardiovascular function was analyzed in rats after vagal stimulation and nitroprusside-induced hypotension. Intermittent cervical vagal stimulation induced a progressive reduction in the levels of extracellular glutamate in the PBN. However, termination of vagal stimulation increased the basal levels of glutamate. Furthermore, elevated glutamate levels after the termination of vagal stimulation altered cardiac baroreflex.

The responses of the cardiac atrioventricular (AV) conduction system to brief vagal stimuli were in situ analyzed in canine heart preparations. Analysis of the time-dependent effects of vagal stimulation in canine hearts indicated the role of brief vagal stimulation in increasing atrium-ventricle (A-V) intervals. The effects of pacing site on vagally mediated A-V prolongation were also mediated by the anterior AV nodal tissue compares to the posterior AV nodal tissue.

A system identification technique involving sympathetic and vagal stimulation was utilized to determine the dynamic interactions of heart rate regulation under conditions of combined sympathetic and vagal stimulation. Heart rate response was enhanced by the simultaneous stimulation of sympathetic and vagal nerves. Furthermore, the bidirectional augmentation of heart rate response under conditions of simultaneous dynamic stimulation of sympathetic and vagal systems was independent of the patterns of input signals.

The interaction between the feeding-inhibitory actions and local gastrointestinal (GI) effects of cholecystokinin (CCK) was analyzed in rats during prolonged liquid glucose intake. Analysis of food intake in rats during selective subdiaphragmatic vagal deafferentation indicated the presence of attenuated CCK activity. Furthermore, total supradiapragmatic vagotomy blocked the feeding-inhibitory actions of CCK and reduced the levels of food intake.

The effects of trigeminal and vagus nerve stimulation on the oropharynx and esophagus was analyzed to determine the role of the cranial nerves in the modulation of esophageal and pharyngeal muscles. Two distinct pharyngoesophageal responses were elicited in human oropharynx and esophagus by the electromagnetic stimulation of the suborbital branch of the trigeminal and vagus nerves. The pharyngoesophageal response to afferent stimulation was also mediated by the neurons of the brain stem swallowing center.

The role of vagal function in the modulation of somatosensory-induced alterations in the power spectral pattern of renal nerve activity was analyzed in spontaneously hypertensive (SHR) and normotensive Wistar rats. Administration of capsaicin increased renal nerve activity and elevated blood pressure in SHR and normotensive Wistar rats. However, renal nerve activity in SHR rats were higher after capsaicin treatments compared to normotensive Wistar rats due to major deficiencies in vagal influence on the renal sympathetic nerve output.

The effects of esophageal vagoafferent stimulation on cardioautonomic responses were analyzed in healthy human males during esophageal electrical stimulation. Electric stimulation of the distal esophagus in normal male subjects enhanced the respiratory driven high-frequency band autospectral power of heart rate variability. However, the chronotropic effects of esophageal vagoafferent stimulation on heart rate were minimal and occurred through a direct, vagally mediated action with vagal esophageal afferents.

The effects of arginine vasopressin (AVP) microinjections or intravenous infusion on the response of nucleus of the solitary tract (NTS) neurons to vagus nerve inputs were analyzed in anesthetized rabbits. Analysis of sinoaortic and vagal denervated anesthetized rabbits after administration of AVP indicated the presence of augmented NTS neuronal response to aortic/vagal stimulation. AVP-mediated enhancement of sympathoinhibitory response to increases in arterial pressure can be inhibited by pretreatment of animals with AVP V1 receptor antagonists.

The effects of pulmonary vagal C fibers with 5-HT3 serotonin receptors in the regulation of renal sympathetic nerve activity (RSNA) were analyzed in male Sprague-Dawley rats. Administration of phenylbiguanidine (PBG) in rats reduced blood pressure (BP), heart rate (HR) and RSNA. However, the effects of PBG on BP and HR were attenuated by intrapericardial procaine which inhibited the activity of cardiac afferents. The effects of PBG indicated the regulatory role of pulmonary serotonin on the RSNA.

The role of vagus nerves and gastrin in the gastric phase of acid secretion was analyzed in urethan-anesthetized male Wistar rats during mechanical and chemical stimulation of the gastric lumen. Analysis of gastric distension in rats after extensive vagotomy indicated the role of vagus nerves in mediating distension-induced acid secretion. Furthermore, vagotomy abolished all basal and distension-induced acid secretion in conscious rats during the gastric phase.

The effects of somatostatin on exocrine pancreatic secretion stimulated by vagal nerve efferent excitation was analyzed in conscious Wistar rats. Intracerebroventricular injections of somatostatin in rats inhibited pancreatic secretions that were induced by thyrotropin-releasing hormones (TRH). Somatostatin also inhibited vagal afferent nerve excitation that was mediated by TRH. Furthermore, 2-deoxy-D-glucose and TRH promote pancreatic secretion by stimulating the vagal efferent nerve via distinct pathways.

Fasted conscious dogs were analyzed during the interdigestive state to determine the relationship between pancreatic polypeptide (PP) and motilin release. Analysis of plasma motilin in PP concentrations in mongrel dogs by radioimmunoassay indicated the role of exogenous motilin in enhancing the release of PP in a dose-dependent manner. The interdigestive cyclic change in PP release was regulated by motilin via vagal, muscarinic and cholinergic pathways involving 5-hydroxytryptamine3 receptors in mongrel dogs.

Gastric acid secretion were analyzed in Danish Landrace pigs after splanchnicotomy to determine the effects of electrical vagal stimulation (EVS) on pancreaticobiliary and duodenal mucosal bicarbonate secretion. Pancreaticobiliary and duodenal mucosal secretion of bicarbonates was significantly enhanced in pigs after EVS. However, administration of atropine inhibited the effects of EVS on mucosal bicarbonate secretion indicating the role of vagal stimulation in mediating bicarbonate secretion in the duodenum and pancreas.

The mechanisms that mediate the intestinal action of cholecystokinin (CCK) and CCK-A receptors during the postprandial disruption of migrating motor complexes (MMC) were analyzed in Sprague-Dawley rats by electromyography. Oral administration of soybean trypsin inhibitor in Sprague-Dawley rats induced the endogenous release of CCK and disrupted MMC. CCK-mediated disruptions of MMC also involves the stimulation of CCK-B receptors in the vagal afferent fibers which initiates a reflex action that is also mediated by the activation of CCK-A receptors.

Open-chest dogs were analyzed to determine the functional role of NO in the autonomic modulation of cardiac-excitable properties such as spontaneous sinus cycle length (SCL) and atrioventricular (AV) nodal conduction time. The negative chronotropic and dromotropic responses of sinus and AV nodal arteries to vagal nerve stimulation was inhibited by N-G-monomethyl-L-arginine in open-chest dogs. Furthermore, NO mediated vagal neurotransmission and inhibited sympathetic neurotransmission.

Urethan-anesthesized rats injected with bombesin (BBS) were analyzed to determine the effect of on cholecystokinin (CCK)-sensitive vagal afferent discharge (GVAD) and gastric distension. Administration of BBS by intravenous injection enhanced multi-unit GVAD by 120%-150% within 60 minutes. Furthermore, intravenous injections of BBC also enhanced pancreatic exocrine secretion which was mediated by CCK. However, BBC-activity on GVAD was inhibited by ICI-21640 desmethionine/BBS receptor antagonist.

The role of parasympathetic neurons in the nucleus ambiguus (NA) on cardiac pacing was analyzed by patch-clamp electrophysiology in parasympathetic cardiac neurons of the dorsal motor nucleus of the vagus (DMNX). The parasympathetic cardiac neurons in the NA did not exhibit phasic depolarizations or action potentials. The lack of pacemaker activity in DMNX neurons was also detected when the neurons remained silent in the absence of synaptic activity.

The effects of intraduodenal infusions of 10 nutrients on the food intake of rats with selective deafferentations of the celiac branches of the vagus nerve were observed to identify the location of the receptors involved in the negative feedback loop that controls food intake. The results show that vagal celiac afferent nerves are involved in the suppression of food intake by preabsorptive detection of certain nutrients.

RX-77368, a stable analogue of thyrotropin-releasing hormone (TRH), was injected into the dorsal motor nucleus of the vagus nerve in rats to determine the role of TRH in protect the stomach against ethanol-induced injury. The results show that low doses of TRH provide gastric protection against ethanol-induced lesions. Gastric protection is effected via nitric oxide-, muscarinic-, calcitonin gene-related peptide- and prostaglandin E2-mediated mechanisms.

The role of the parasympathetic input to the sinus node for the regulation of heart rate was examined using anesthetized dogs prepared in a synchronized vagal stimulation setup. The results indicate that the heart rate response to synchronized vagal stimulation has a slow and fast component, the magnitudes of which depend on the mean level of vagal tone. Furthermore, the fast component is linked to beat-to-beat variations in the heart rate.

The pancreatic polypeptide hormone induces the secretion of gastric acid through the dorsal vagal complex. Rats injected with 100 parts per mol of pancreatic polypeptide raised their levels of gastric acid significantly above the baseline levels, and this effect was minimized by cutting the cervical vagus bilaterally or by treatment with atropine. In addition, the effective dose of pancreatic polypeptide necessary to induce a response was determined to be between 10 and 100 ppmol.

The vagus nerve seems to be responsible for regulating the blood pressure in the hearts of unanaesthesized and freely moving rats. The effects of the efferent vagal innervation was determined by blockage with atropine and propranolol, where blockage was not complete when the substances were used in isolation. However, atropine was able to alter mean arterial pressure and the median and high-frequency responses of the heart.

A study conducted on anesthetized pigs shows that the efferent vagal nerve controls pyloric resistance which determines the flow of liquids from the stomach. Stimulation of the cervical and thoracic vagi nerve increases transpyloric liquid flow by decreasing pyloric resistance and antral wall tension. This increased flow is accompanied by an increase in antropyloroduodenal pressure. Vagotomy has no effect on pyloric resistance but it reduces gastric emptying of liquids antral pressure and pyloric pressure events.

There is mounting evidence that interleukin -1beta is a neural transmitter in the brain stem. A study of the influence on thyrotropin releasing hormone (TRH) analogue (RX-77368)-induced boosting of gastric contractility by murine interleukin-1-beta (mIL-1-beta) microinserted into the dorsal vagal complex (DVC) of fasted, anaesthetized rats show that mIL-1-beta initiates suppression of vagally stimulate gastric contractility in the DVC which is mediated by IL-1 receptors.

A new surgical procedure helps generate rats having bilaterally deafferented but only unilaterally deefferented subdiaphragmatic vagus or vice versa. Histological assessment helps check the completion of transections and microscopic inspection helps determine the adequacy of the contralateral subdiaphragmatic vagotomy. Absence of fibers connecting proximal and distal cut ends reveals the completion of unilateral vagotomy.

A study of the effect of vagal nerve stimulation on pulmonary and systemic blood circulations in the turtle Pseudemys scripta reveals that adrenergic and cholinergic mechanisms produce reciprocal changes in heart rate (HR), pulmonary blood flow (Qpul) and pulmonary vascular resistance (Rpul). Efferent vagal stimulation results in cholinergic responses that cause reductions in the HR and Qpul followed by an increase in Rpul with net R-L shunt development. Afferent vagal stimulation leads to an adrenergic response that results in increase of HR, Qpul and reduction in Rpul with the onset of a large net R-L shunt.

Study of the influence of amylin on food intake in mice aged four to 22 months after vagotomy reveals that vagus has no influence on the amylin induced anorexic effect, independent of the release of cholecystokinin. Reduced food intake due to amylin is the same for obese and lean mice. Food intake decreases in older animals, accompanied by loss of weight due to a central opioid feeding drive decrease and an enhanced satiety effect.

Interactions of cholecystokinin (CCK) with vagal low-affinity CCK-A receptor mediate the vagal afferent responses to CCK in a population of rat gastric mechano-sensitive fibers. Partial functional separation between neurophysiological responses from gastric distension and those from CCK shows the involvement of transduction mechanisms in these responses.

Vagal stimulation induces a negative inotropic effect on the left ventricle (LV) myocardium even after cardiac sympathetic denervation and beta-adrenergic inhibition. Vagal stimulation alters the filling mode of the left ventricle due to variations in left atrial (LA) contractivity and pressure. Vagal stimulation of LV contraction is independent of its effects on heart rate and LV loading conditions.

Research on the influence of vagus nerve and the serotonin3 (5-HT3) receptor on the mediation of food intake depression, related to amino acid inadequacy in rats fed with isoleucine-imbalanced (IMB) diet, reveals an increase in IMB intake due to 5-HT3 antagonist tropisetron treatment. The vagal physiological system participates in the anorectic responses to IMB. Establishment of the complete effect of 5-HT3 antagonists in the weakening of anorectic response to IMB requires intact vagal function.

Cardiopulmonary receptor vagal efferents may reduce arterial baroreceptor induced sympathetic activation. This occurs during air injection induced hypotension. The lethal changes that take place during venous air embolism are overcome by the action of arterial baroreceptor nerves. All animals with cervical vagotomy survived.

Studies on endogenous acetylcholine release in cat ventricles suggest that acetylcholine (ACh) release from the postganglionic vagal nerves of the left ventricular myocardium affect dialysate ACh levels. The use of a dialysis technique enables the estimation of efferent cardiac vagal nerve activity fluctuations. The increase in ACh values from 588 plus or minus 211 pM in controls is 9,366 plus or minus 1,873 pM at 10Hz.

An analysis of the possible role of nitric oxide as an intercellular messenger in the dorsal motor nucleus (DMV) of rat vagus confirms the existence of NO synthase (NOS) in DMV neurons. Formation of NO and subsequent accumulation of cGMP in DMV neurons is partially responsible for the excitatory influence of N-methyl-D-aspartate. The extracellular cell-altered recording is used to study DMV motoneurons of rats.

Arrythmogenic reaction of phasic vagal stimuli with atrial ectopic pacemakers is modeled by a computer algorithm. Conducting atrial tissue is used to isolate the solitary ectopic pacemaker core, which, with a dominant sinus rode, forms the model. Timing and occurrence of atrial premature beats are hypothesized by the model. Induction of the vagal-stimulated entrance obstacle of the sinus impulse near the ectopic focus causes the beats. A sequence of experimentally obtained phase-reaction and rectified retrieval time curves are used to make the predictions. Vagal input and overdrive restraint are used to determine the regulation of ectopic pace-maker periodicity.

The G(o) and G(i) proteins in the cardiac muscles undergo ADP ribosylation due to the in vivo addition of pertussis toxin. The cardial vagal regulation of the rate of the heart increases due to the ADP ribosylation. Cardial muscarinic receptors are damaged by the pertussis toxin, causing an increase in the physiological vagal monitoring of the heart rate in dogs. G protein in vitro synthesis cause alterations which are connected to the influences of pertussis toxin. The cardiac vagal reactions are systematically prevented by pertussin toxin.

Nervous regulation of duodenal bile perfusion between and during digestive periods was investigated in conscious dogs using cold blockade and cervical vagosympatheticnerve transection techniques. Results reveal that the cervical vagosympathetic nerve has an important regulatory function in partial gall bladder emptying in between digestive periods. It also mediates the cephalic phase of duodenal bileperfusion as well as the cholecyctokinin-induced contraction of the gall bladder.

The influence of distention of anintestinal segment on water absorption at another segment noncontinuous with the distended region was investigated in rats. Results show that absorption in the noncontiguous segment is promoted by intestinal distention in subjects withsevered splanchnic nerves and intact vagi. Further, neural activity was reducedin 24 out of 26 vagal efferents after intestinal distention. This effect was abolished in subjects with transected afferent vagi. This suggests that distention activates a vagal circuit in subjects with trasected splanchnic nerves.

A study to pinpoint the site of origin of the inhibitory effect of glucagon on spontaneous feeding in rats and to test the dependency of glucagon satiety on the vagus nerve is presented. The study protocol involved glucagon infusion into either the hepatic portal vein or the inferior vena cava during spontaneous feeding and glucagon infusion into hepatic vagotomized rats andintact rats. The results indicate that glucagon acts on receptors in the liver, which transmits a satiety signal to the brain via the hepatic branch of the abdominal vagus nerve.