Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Smooth muscle specimens were taken from the lower esophageal sphincter of patients suffering from achalasia or hiatus hernia with gastro-esophageal reflux. The specimens were analysed for neurohormonal peptides using immunochemistry and immunocytochemistry. Control specimens were obtained from patients subjected to esophageal resection because of esophageal cancer. The concentration of vasoactive intestinal polypeptide (VIP) was higher and the VIP nerve supply greater in patients with hiatus hernia than in control patients. The VIP nerve supply and the content of this peptide was lower in patients with achalasia than in controls. The same tendency was observed for substance P and enkephalin although the changes in their concentrations were not statistically significant. Enkephalin fibers were few, both in specimens from control patients and from patients with hiatus hernia; they could not be detected in specimens from patients with achalasia. Never fibers containing somatostatin or gastrin/cholecystokinin could not be detected in any of the groups and somatostatin and gastrin/cholecystokinin could not be measured in extracts of the lower esophageal sphincter. We propose that changes in the concentration of neuropeptides may at least contribute to manifestations of achalasia and of decreased lower esophageal sphincter pressure and gastro-esophageal reflux.
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PMID:Regulatory peptides in the lower esophageal sphincter of man. 258 Dec 86

Gastroesophageal reflux disease (GERD) afflicts approximately 20% of adults in the United States on a weekly basis and 40% on a monthly basis, and is also a trigger for asthma. The prevalence of GERD is higher in asthmatics compared to control groups, with 77% of asthma patients having reflux symptoms and 82% of asthmatics having abnormal esophageal acid contact times on 24-hour esophageal pH testing. Esophageal acid elicits respiratory responses including decreases in airflow, oxygen saturation, and increases in respiratory resistance, minute ventilation, and respiratory rate. Mechanisms of esophageal acid-induced bronchoconstriction include a vagally-mediated reflex, heightened bronchial reactivity, and microaspiration. Esophageal acid also produces airway neurogenic inflammatory responses with the release of substance P, tachykinins, nitric oxide, and other cytokines. Predisposing factors to GERD development in asthmatics include autonomic dysregulation, an increased pressure gradient between the thorax and the abdomen, a high prevalence of hiatal hernia, and altered crural diaphragm function. Theophylline may also potentiate GERD. Therapy of GERD improves asthma outcome. In combined studies examining 326 medically treated asthma patients, asthma symptoms improved in 69% of patients. Surgical therapy trials in 417 asthma patients show asthma symptoms improved in 79%. Management strategies for GERD in asthmatics with reflux symptoms include utilizing an empiric trial of a proton pump inhibitor for three months while measuring asthma outcomes. Since GERD may be clinically ''silent'' in asthma patients, consider 24-hour esophageal pH testing in severe asthma patients who do not have GERD symptoms. Future research will develop the association between asthma and GERD.
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PMID:The potential role of gastroesophageal reflux in asthma. 1649 63