Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0014848 (achalasia)
 2,804 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasoactive intestinal polypeptide (VIP) is one of the main neurotransmitters implicated in the relaxation of the lower esophageal sphincter (LES). The effect of exogenous VIP on LES motor activity was determined by esophageal manometry. LES pressure (LESP) and LES relaxation were compared in four healthy volunteers and in six patients with achalasia. The effects of intravenous doses of 1.5, 3, and 5 pmol.kg-1.min-1 of VIP were compared with placebo. Neither placebo nor 3 and 5 pmol.kg-1.min-1 of VIP produced any effect on esophageal motility in healthy volunteers. In achalasia the three doses of VIP caused a dose-dependent decrease in LESP with a significant improvement in LES relaxation. A dose of 5 pmol.kg-1.min-1 produced a maximal decrease of 51% in LESP. A beta-adrenergic agonist, isoproterenol, caused a decrease in LESP both in healthy volunteers and in patients with achalasia without improving LES relaxation. In summary, intravenous VIP improved LES relaxation and caused a decrease in LESP in patients with achalasia without affecting LESP in healthy volunteers, indicating that the LES muscle in achalasia is supersensitive to VIP. The current study suggests that a selective damage in the noncholinergic nonadrenergic innervation of the esophagus is in part responsible for the motor alteration seen in these patients. The findings and the inability of isoproterenol to improve LES relaxation despite decreasing LESP support a role in VIP as a indicator of LES relaxation.
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PMID:The effect of vasoactive intestinal polypeptide on the lower esophageal sphincter in achalasia. 163 56

Vasoactive intestinal polypeptide (VIP) has been postulated as a neuropeptide with inhibitory neurotransmitter activity in nonadrenergic noncholinergic pathways. Transcutaneous electric nerve stimulation (TENS) relaxes the lower esophageal sphincter in patients with achalasia. Such response is accompanied by a 30% increase in VIP concentrations in the systemic circulation. Since the sphincter of Oddi (SO) receives a very dense VIP nerve supply, we evaluate the effect of TENS on SO motor activity and on VIP plasma concentrations in patients with biliary dyskinesia and in healthy volunteers. TENS was performed with a pocket stimulator for 45 min. SO pressure and VIP levels were obtained before and after 45 min of TENS. In patients with SO dyskinesia, TENS produced a significant decrease in SO pressure from 80.1 +/- 11.9 mm Hg to 58.3 +/- 9.7 mm Hg p less than 0.01); this was accompanied by a significant increase in VIP plasma levels from 21.1 +/- 0.5 pg/ml to 32.6 +/- 1.5 pg/ml (p less than 0.01). In healthy volunteers, TENS did not produce significant changes in SO pressure. However, a significant increase in VIP plasma values was observed (p less than 0.01). No significant changes in amplitude, duration and frequency of SO phasic contractions were observed in either of the two groups evaluated. We conclude that, in patients with SO dyskinesia, TENS decreases SO basal pressure, possibly by a direct action of the released VIP in the systemic circulation. In healthy volunteers, TENS increases VIP plasma values without significant effect on SO basal pressure. These findings suggest that the response to TENS may be mediated by VIP. It is also possible that the alterations seen in patients with biliary dyskinesia may be due to impairment of the VIP nerve supply at the level of the SO.
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PMID:The effect of transcutaneous nerve stimulation on sphincter of Oddi pressure in patients with biliary dyskinesia. 202 48

Vasoactive intestinal polypeptide-containing nerves were examined in the lower esophagus of control and achalasia patients. The smooth muscle in patients with achalasia had conspicuously fewer vasoactive intestinal polypeptide-immunoreactive nerve fibers than specimens from control patients. Also the concentration of vasoactive intestinal polypeptide in the lower esophagus was much reduced in achalasia. In view of the potent smooth muscle relaxing effects of vasoactive intestinal polypeptide, it is suggested that the reduced number of vasoactive intestinal polypeptide fibers in the achalasic esophagus causes or at least contributes to the incomplete relaxation and the increased resting tone of the lower esophageal sphincter characteristic of this disease.
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PMID:Lack of vasoactive intestinal polypeptide nerves in esophageal achalasia. 683 68

Transcutaneous stimulation (TNS) at esophageal acupuncture points decreases lower esophageal sphincter (LES) pressures in patients with achalasia. We examined the effect of TNS on esophageal motility and vasoactive intestinal peptide (VIP) levels in normal subjects. TNS was applied to either hand or foot (placebo) in 10 volunteers. Esophageal and LES pressures were recorded and blood was drawn for VIP analysis. Hand TNS improved LES relaxation and percent of peristaltic contractions to swallows, and decreased the number of spontaneous contractions. Foot TNS decreased only spontaneous contractions while LES pressures and VIP levels were unchanged. We conclude that a somatovisceral pathway involving the esophagus exists.
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PMID:Effect of transcutaneous nerve stimulation on esophageal function in normal subjects--evidence for a somatovisceral reflex. 887 76