Role of capsaicin-sensitive afferent neurons in receptive relaxation induced by gastric distension in rats

2007 ◽  
Vol 15 (6) ◽  
pp. 273-277 ◽  
Author(s):  
M. Taniguchi ◽  
Y. Mashita ◽  
Y. Matsuzaka ◽  
S. Kato ◽  
K. Takeuchi
Keyword(s):  
Gastric Distension ◽  
Afferent Neurons ◽  
Receptive Relaxation

scholarly journals Tetrodotoxin: A New Strategy to Treat Visceral Pain?

Toxins ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 496
Author(s):  
Ana Campos-Ríos ◽  
Lola Rueda-Ruzafa ◽  
Salvador Herrera-Pérez ◽  
Paula Rivas-Ramírez ◽  
José Antonio Lamas
Keyword(s):  
Action Potentials ◽  
Channel Blocker ◽  
Visceral Pain ◽  
Visceral Hypersensitivity ◽  
Afferent Neurons ◽  
Sodium Channel Blocker ◽  
Voltage Gated Sodium Channels ◽  
New Strategy ◽  
Specific Receptors

Visceral pain is one of the most common symptoms associated with functional gastrointestinal (GI) disorders. Although the origin of these symptoms has not been clearly defined, the implication of both the central and peripheral nervous systems in visceral hypersensitivity is well established. The role of several pathways in visceral nociception has been explored, as well as the influence of specific receptors on afferent neurons, such as voltage-gated sodium channels (VGSCs). VGSCs initiate action potentials and dysfunction of these channels has recently been associated with painful GI conditions. Current treatments for visceral pain generally involve opioid based drugs, ≠≠which are associated with important side-effects and a loss of effectiveness or tolerance. Hence, efforts have been intensified to find new, more effective and longer-lasting therapies. The implication of VGSCs in visceral hypersensitivity has drawn attention to tetrodotoxin (TTX), a relatively selective sodium channel blocker, as a possible and promising molecule to treat visceral pain and related diseases. As such, here we will review the latest information regarding this toxin that is relevant to the treatment of visceral pain and the possible advantages that it may offer relative to other treatments, alone or in combination.

scholarly journals Anatomy and physiology of phrenic afferent neurons

2017 ◽  
Vol 118 (6) ◽  
pp. 2975-2990 ◽  
Author(s):  
Jayakrishnan Nair ◽  
Kristi A. Streeter ◽  
Sara M. F. Turner ◽  
Michael D. Sunshine ◽  
Donald C. Bolser ◽  
...  
Keyword(s):  
Potential Role ◽  
Large Diameter ◽  
Respiratory Cycle ◽  
Conscious Perception ◽  
Relative Impact ◽  
Afferent Neurons ◽  
Sensory Afferents ◽  
Synaptic Contacts ◽  
Anatomy And Physiology

Large-diameter myelinated phrenic afferents discharge in phase with diaphragm contraction, and smaller diameter fibers discharge across the respiratory cycle. In this article, we review the phrenic afferent literature and highlight areas in need of further study. We conclude that 1) activation of both myelinated and nonmyelinated phrenic sensory afferents can influence respiratory motor output on a breath-by-breath basis; 2) the relative impact of phrenic afferents substantially increases with diaphragm work and fatigue; 3) activation of phrenic afferents has a powerful impact on sympathetic motor outflow, and 4) phrenic afferents contribute to diaphragm somatosensation and the conscious perception of breathing. Much remains to be learned regarding the spinal and supraspinal distribution and synaptic contacts of myelinated and nonmyelinated phrenic afferents. Similarly, very little is known regarding the potential role of phrenic afferent neurons in triggering or modulating expression of respiratory neuroplasticity.

Gastroprotective and vasodilatory effects of epidermal growth factor: the role of sensory afferent neurons

2001 ◽  
Vol 280 (5) ◽  
pp. G897-G903 ◽  
Author(s):  
Yoji Matsumoto ◽  
Kohki Kanamoto ◽  
Keishi Kawakubo ◽  
Hitoshi Aomi ◽  
Takayuki Matsumoto ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Mucosal Injury ◽  
Protective Role ◽  
Sensory Nerves ◽  
Afferent Neurons ◽  
Gastric Mucosal Lesions ◽  
Calcitonin Gene ◽  
Epidermal Growth

Epidermal growth factor (EGF) has been shown to exert gastric hyperemic and gastroprotective effects via capsaicin-sensitive afferent neurons, including the release of calcitonin gene-related peptide (CGRP). We examined the protective and vasodilatory effects of EGF on the gastric mucosa and its interaction with sensory nerves, CGRP, and nitric oxide (NO) in anesthetized rats. Intragastric EGF (10 or 30 μg) significantly reduced gastric mucosal lesions induced by intragastric 60% ethanol (50.6% by 10 μg EGF and 70.0% by 30 μg EGF). The protective effect of EGF was significantly inhibited by pretreatment with capsaicin desensitization, human CGRP1 antagonist hCGRP-(8–37), or N ω-nitro-l-arginine methyl ester (l-NAME). Intravital microscopy showed that topically applied EGF (10–1,000 μg/ml) dilated the gastric mucosal arterioles dose dependently and that this vasodilatory effect was significantly inhibited by equivalent pretreatments. These findings suggest that EGF plays a protective role against ethanol-induced gastric mucosal injury, possibly by dilating the gastric mucosal arterioles via capsaicin-sensitive afferent neurons involving CGRP and NO mechanisms.

scholarly journals Gastric branch vagotomy and gastric emptying during and after intragastric infusion of glucose

1997 ◽  
Vol 273 (5) ◽  
pp. R1786-R1792 ◽  
Author(s):  
Joel M. Kaplan ◽  
William H. Siemers ◽  
Ulrika Smedh ◽  
Gary J. Schwartz ◽  
Harvey J. Grill
Keyword(s):  
Gastric Emptying ◽  
Feedback Control ◽  
Inhibitory Control ◽  
Inhibitory Mechanisms ◽  
Two Phases ◽  
And Control ◽  
Vagal Efferents ◽  
Receptive Relaxation ◽  
Over Time

The effect of gastric branch vagotomy (GVX) on the gastric emptying of glucose was evaluated during two phases of emptying control: as the stomach fills and in the postload period. GVX and control rats received a series of intragastric glucose infusions (1.0 ml/min) through indwelling gastric fistulas. In experiment 1, gastric samples were withdrawn either immediately after the offset of 9- or 18-min infusions of 12.5% glucose or at various times up to 36 min postinfusion. In experiment 2, samples were withdrawn either immediately or 30 min after termination of 12-min infusions of 12.5 or 25% glucose. After gastric fill, glucose solute emptying rate was stable over time, not influenced by concentration doubling, and, surprisingly, not affected by GVX. During gastric fill, solute emptying rate doubled with concentration in both GVX and control rats. For each concentration, however, glucose emptied during fill at almost twice the rate in GVX compared with control rats. This accelerated emptying of glucose during fill in GVX rats is consistent with a gastric vagal contribution to inhibitory mechanisms (e.g., receptive relaxation) that operate as the stomach fills under normal conditions. The absence of a GVX effect on emptying after fill suggests either that gastric branch vagal efferents play little role in feedback inhibitory control of glucose emptying under normal conditions or that other systems compensate for the function previously served by vagal gastric branch efferents. Further work is required to address the possible role of the gastric vagus in feedback control of gastric emptying when nutritive fluids other than glucose are delivered.

H. pylori and transient lower esophageal sphincter relaxations induced by gastric distension in healthy humans

2001 ◽  
Vol 281 (2) ◽  
pp. G350-G356 ◽  
Author(s):  
Frank Zerbib ◽  
Valérie Bicheler ◽  
Véronique Leray ◽  
Madeleine Joubert ◽  
Stanislas Bruley des Varannes ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Lower Esophageal Sphincter ◽  
Proinflammatory Cytokine ◽  
Healthy Subjects ◽  
Gastric Distension ◽  
Healthy Humans ◽  
Biopsy Specimens ◽  
Esophageal Sphincter ◽  
H Pylori

The role of Helicobacter pylori infection in the control of lower esophageal sphincter (LES) motility, especially the occurrence of transient LES relaxations (TLESRs), was studied in eight H. pylori-positive and eight H. pylori-negative healthy subjects. During endoscopy, biopsy specimens were taken from the cardia, fundus, and antrum for determinations of H. pyloristatus, gastritis, and proinflammatory cytokine mucosal concentrations. LES motility was monitored during three different 30-min periods: baseline, gastric distension (barostat), and gastric distension with CCK infusion. Gastric distension significantly increased the TLESR rate, whereas CCK increased the rate of distension-induced TLESRs further and reduced resting LES pressure without significant differences between infected and noninfected subjects. H. pylori status did not influence resting LES pressure or gastric compliance. Cytokine mucosal concentrations were increased in infected patients, but no correlation was found with the TLESR rate, which was also independent of inflammation at the cardia, fundus, and antrum. These results suggest that H. pylori-associated inflammation does not affect the motor events involved in the pathogenesis of gastroesophageal reflux.

Haemodynamic Effects of Eating: The Role of Meal Composition

1996 ◽  
Vol 90 (4) ◽  
pp. 269-276 ◽  
Author(s):  
U. Høst ◽  
H. Kelbaek ◽  
H. Rasmusen ◽  
M. Court-Payen ◽  
N. Juel Christensen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Portal Vein ◽  
Forearm Blood Flow ◽  
Plasma Catecholamines ◽  
Left Ventricular ◽  
Gastric Distension ◽  
Left Ventricular Volumes ◽  
Portal Vein Flow

1. The purpose of this study was to investigate the effect of fractional meal stimulation on postprandial haemodynamic changes, the possible correlation between these changes and the potential mediating role of circulating catecholamines and insulin. 2. Healthy young subjects were studied before and after ingestion of isocaloric, isovolumetric high-protein, carbohydrate or fat meals (80–85% of total energy), 60 kJ per kg of body weight. Multigated radionuclide cardiography with autologous 99mTc-labelled erythrocytes was performed for assessment of cardiac output, venous occlusion plethysmography to obtain forearm blood flow and Doppler-ultrasonography for portal vein flow. Plasma levels of catecholamines and insulin were determined by radioimmunoassay. 3. Cardiac output increased considerably after each meal, including the control meal (water) with only minor differences in extent and timing. Left ventricular volumes increased after food intake, most pronounced after carbohydrate and protein. Forearm blood flow increased only after carbohydrate and protein. Portal vein flow increased after all meals, especially after fat, but also after the control meal. There was a significant correlation between the increment in cardiac output and changes in forearm and portal vein flow, but no correlation between either haemodynamic response and plasma catecholamines or insulin. 4. Postprandial cardiovascular changes are not substantially different after various isocaloric and isovolumic meal compositions. Gastric distension seems to play a role in the increase in cardiac output, accomplished by ventricular dilatation. These changes seem to some extent to be linked to changes in muscle and splanchnic flow.

Gastroprotective Effect of the Mixture of α- and β-Amyrin fromProtium heptaphyllum: Role of Capsaicin-Sensitive Primary Afferent Neurons

Planta Medica ◽  
2004 ◽  
Vol 70 (8) ◽  
pp. 780-782 ◽  
Author(s):  
Francisco A. Oliveira ◽  
Gerardo M. Vieira-Júnior ◽  
Mariana H. Chaves ◽  
Fernanda R. Almeida ◽  
Kelcyana A. Santos ◽  
...  
Keyword(s):  
Afferent Neurons ◽  
Primary Afferent Neurons ◽  
Primary Afferent ◽  
Gastroprotective Effect
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