Non-adrenergic Inhibitory Fibres Research Articles

Autonomic innervation of the ovary of the Atlantic cod,Gadus morhua

The autonomic innervation of the ovary of the Atlantic cod was investigated using histochemical and physiological/pharmacological methods. The paired ovary receives autonomic innervation via branches of the posterior splanchnic nerve (vesicular nerve).Histochemical studies demonstrated vasoactive intestinal polypeptide (VIP)-immunoreactive, 5-hydroxytryptamine-immunoreactive and adrenergic nerve fibers, but a number of antisera raised against other peptides failed to reveal any specific reaction in the tissue preparations. It is concluded that the cod ovary receives a double antagonistic autonomic innervation of excitatory cholinergic fibers and non-adrenergic inhibitory fibers. The nature of the inhibitory neurotransmitter is not known.

Regulatory peptides in the respiratory system.

Many regulatory peptides have been described in the respiratory tract of animals and humans. Some peptides (bombesin, calcitonin, calcitonin gene-related peptide) are localised to neuroendocrine cells and may have a trophic or transmitter role. Others are localised to motor nerves. Vasoactive intestinal peptide and peptide histidine isoleucine are candidates for neurotransmitters of non-adrenergic inhibitory fibres and may be cotransmitters in cholinergic nerves. These peptides may regulate airway smooth muscle tone, bronchial blood flow and airway secretions. Sensory neuropeptides (substance P, neurokinin A and B, calcitonin gene-related peptide) may contract airway smooth muscle, stimulate mucus secretion and regulate bronchial blood flow and microvascular permeability. If released by an axon reflex mechanism these peptides may be involved in the pathogenesis of asthma. Other peptides, such as galanin and neuropeptide Y, are also present but their function is not yet known.

Reflex control of the gastric motility by the vagus and splanchnic nerves in the guinea pig in vivo

Gastric responses to electrical stimulation of the vagus and splanchnic nerves and to esophageal distension were observed in studies of the reflex control of the gastric motility in anesthetized guinea pigs in vivo. The gastric motility was inhibited by both vago-vagal and splanchno-vagal reflexes through the activation of non-adrenergic inhibitory nerve fibers and by splanchno-splanchnic reflex through the inactivation of the intramural cholinergic excitatory neurons. Distension of the lower esophagus caused a relaxation of the stomach which was mediated by an intrinsic reflex via intramural non-adrenergic inhibitory neurons. Furthermore, stimulation of the splanchnic nerve innervating the stomach seems to activate adrenergic inhibitory, cholinergic excitatory and probably some non-adrenergic inhibitory fibers.

P-428) - Possibility of the existence of non-adrenergic inhibitory fibers in the sympathetic nerve innervating the guinea pig stomach

P-428) - Possibility of the existence of non-adrenergic inhibitory fibers in the sympathetic nerve innervating the guinea pig stomach

The role of the vagus and splanchnic nerves in the regulation of intragastric pressure in the ferret.

1. The role of the vagus and splanchnic nerves in the regulation of intragastric pressure was investigated by quantifying the effect of nerve section on the response to a standard fluid inflation of the stomach. An opportunity was also taken to compare the responses to a step and physiological ramp inflation of the same volume (50 ml). 2. The peak pressure at the end ot the step inflation (13.6 +/- 1.0 cmH2O) was twice that for a ramp inflation (6.2 +/- 0.4 cmH2O). 5 min after the peak the pressures were similar (4.8 +/- 0.3 cmH2O; 4.7 +/- 0.3 cmH2O) for both. 3. Vagotomy produced a significant increase in the intragastric pressure response for both the peak and plateau levels of the step and ramp inflations. 4. Atropine produced a statistically significant decrease in the pressure response to both step and ramp inflation. 5. Splanchnic nerve section produced an increase in the intragastric pressure response to both step and ramp inflations although the values failed to reach the 5% significance level. However, following vagotomy or atropine, section of the splanchnic nerves produced a statistically significant increase in the pressure response to inflation. 6. These results indicate that the vagal cholinergic excitatory and vagal non-cholinergic, non-adrenergic inhibitory fibres are activated at physiological levels of gastric inflation and play a role in the regulation of intragastric pressure. The splanchnic nerves also play a role although in the intact animal they are suppressed by the action of the vagus nerve.

Reflex vagal inhibition of gastric motility by intestinal nociceptive stimulation in the cat.

The effect on gastric motility of various irritative stimuli to the small and large intestine and peritoneum were studied in anesthetized cats. Mechanical stimulation of the jejunum or colon elicited gastric relaxation, which was not blocked by antiadrenergic or anticholinergic drugs but was abolished by vagotomy. Long-lasting gastric relaxation with similar characteristics was observed on jejunal surgery, spontaneous peritonitis, or chemical irritation of the abdominal cavity with acid or methanol. Diathermic lesions of the gut caused less gastric inhibition than mechanical and chemical stimuli. Afferent electric stimulation of jejunal and colonic nerves induced gastric relaxation with similar characteristics as mechanical stimulation in the same regions. It is concluded that mechanical and chemical irritation of the gut and intestinal surgery and peritonitis are accompanied by a gastric relaxation due to activation of the vagal nonadrenergic inhibitory fibers to the stomach. This vagal mechanism is suggested to be important for the suppression of gastric motility in paralytic ileus.

Spino-vagal nonadrenergic inhibition of gastric motility elicited by abdominal nociceptive stimulation in the cat.

Reflex inhibition of gastric motility in response to intestinal nociception and afferent nerve stimulation was studied in anesthetized cats. Mechanical stimulation of the small and large intestines elicited marked gastric inhibition, which was imitated by direct electrical stimulation of mesenteric or splanchnic afferents. The reflex response was resistant to atropine, guanethidine, and adrenalectomy. Spinal cord transection at the cervical level or spinal anesthesia completely blocked the reflex, as did vagotomy or vagal cold blockade. Chemical peritoneal stimulation by hydrochloric acid induced long-lasting gastric inhibition, which was not blocked by antiadrenergic or anticholinergic drugs. This response was reduced, but not completely blocked by spinal anesthesia or spinal cord transection. It is concluded that various nociceptive intestinal stimuli suppress gastric motility via a spino-vagal reflex mechanism composed of spinal afferents in the sympathetic nerves, spinobulbar ascending pathways, and vagal nonadrenergic inhibitory fibers to the stomach. In addition, vago-vagal reflexes evidently contribute to the gastric suppression induced by diffuse peritoneal irritation. These two reflex mechanisms are suggested to be mainly responsible for postoperative gastric inhibition, together with sympatho-adrenergic reflexes.

Pathways for excitatory and inhibitory innervation to the guinea-pig tracheal smooth muscle

The trachea receives excitatory cholinergic innervation from the vagus nerve and the stellate ganglion. Inhibitory adrenergic fibres have the same sources. Those in the vagus nerve probably derive from high vagosympathetic anastomoses. Nonadrenergic inhibitory fibres have a preganglionic vagal supply.

Reflex Suppression of Gastric Motility dúring Laparotomy and Gastroduodenal Nociceptive Stimulation

The effects on gastric motility of laparotomy or of nociceptive stimuli directed to the antro-duodenal area were studied in anaesthetized cats. A diathermic lesion of the duodenal or gastric antral wall induced pronounced gastric relaxation, which could either fade off within 0.5--1.5 h or persist for several hours. This gastric relaxatory response persisted after administration of antiadrenergic and anticholinergic drugs but was eliminated by vagotomy or cold blockade of the vagi. Vagotomy performed during the relaxed gastric state after diathermy immediately resulted in a more or less complete recovery of gastric tone. Blunt mechanical stimulation of the duodenum also caused a prompt gastric relaxation, which showed the same characteristics as the response to diathermy as regards the effects of nerve-blocking drugs and vagotomy. The laparotomy incision per se caused temporary inhibition of rhythmic gastric contraction, but this effect was largely abolished if atropine or guanethidine had been given. It is concluded that nociceptive stimuli against the gastric or duodenal wall induce, besides a sympathoadrenergic reflex inhibition of gastric motility, a profound long-lasting gastric relaxation via a reflex activation of the vagal nonadrenergic inhibitory fibres. This vagally mediated relaxation of the stomach is likely to contribute to the suppression of gastric motility seen in 'paralytic ileus'.

Interactions between vagus nerve stimulation and pentagastrin or secretin on the guinea pig gallbladder.

In guinea pigs, anaesthetised with urethane, stimulation of the peripheral cut end of the cervical vagus activates cholinergic excitatory and non-adrenergic inhibitory fibres to the gallbladder. Central vagal stimulation reflexly contracts the gallbladder by an efferent pathway in the vagus and also activates an adrenergic, non-vagal inhibitory pathway to the gallbladder. Injections of pentagastrin (12-33 mug kg-1 s.c.) or secretin (0.1-0.2 U kg-1 i.a.), doses which produce no effect on gallbladder tone when administered alone, significantly increase the contractions evoked by vagal stimulation.

The presence of inhibitory nerves in the colon after sympathetic denervation

Transmission from intrinsic inhibitory neurons to the guinea-pig colon was examined electrophysiologically before and after sympathetic denervation. Following denervation, all fluorescent noradrenergic nerves disappeared, but the intrinsic inhibitory innervation remained. Pelvic nerve stimulation was purely excitatory. It is concluded that non-adrenergic inhibitory fibres are involved in completely intrinsic control of colonic activity.