Ingestion of elevated amounts of ethanol in humans and rodents induces hemorrhagic gastric lesions, at least in part by increasing oxidative stress. The present study was undertaken in order to evaluate the influence of a bicarbonate-alkaline mineral water (Uliveto on ethanol-induced hemorrhagic gastric lesions in mice. Lesions were evaluated by both macroscopic and microscopic analysis.
View Article and Find Full Text PDFBackground And Aims: It has recently been described that bradykinin B(2) receptors are expressed in the human gallbladder and that their activation induces a powerful contraction, especially in acute cholecystitis tissues. Here the role of the B(1) receptor in the contractility of control and inflamed human gallbladder was investigated.
Methods: Strips of human gallbladder from either acute gallstone cholecystitis or elective gastro-entero-pancreatic surgery (control) were assessed in vitro and processed for reverse transcription-PCR analysis.
Increased resistance in the small airways is a major contributor of airway obstruction in asthma. The role of leukotrienes (LT) in determining inflammation and obstruction of small size bronchi is not completely understood. Here, we have examined the effect of the cysteinyl-leukotriene (CysLT 1) receptor antagonist, montelukast, against the bronchoconstriction and inflammatory responses induced by exogenous leukotriene and by allergen challenge in small size (
Although neurokinin 1 receptor antagonists prevent ethanol (EtOH)-induced gastric lesions, the mechanisms by which EtOH releases substance P (SP) and SP damages the mucosa are unknown. We hypothesized that EtOH activates transient receptor potential vanilloid 1 (TRPV1) on sensory nerves to release SP, which stimulates epithelial neurokinin 1 receptors to generate damaging reactive oxygen species (ROS). SP release was assayed in the mouse stomach, ROS were detected using dichlorofluorescein diacetate, and neurokinin 1 receptors were localized by immunofluorescence.
View Article and Find Full Text PDFObjectives: Adrenergic alpha(1)-receptors agonists and antagonists have been reported to increase and reduce, respectively, neurogenic inflammatory responses mediated by capsaicin-sensitive sensory neurons. However, the precise role and localization of the alpha(1)-adrenoceptors involved in these effects are not known.
Methods: We have studied in the rat whether functional alpha(1)-adrenoreceptors are expressed in primary sensory neurons, and whether they regulate neurogenic inflammation and nociceptive responses in the urinary bladder.