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Results for “INTESTINAL SECRETIONS”

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At least 1,711 records · Page 95Linked to original sources
PubMed1990

Evidence for chloride secretion in the intestine of the winter flounder.

The effects of a novel antisecretory peptide (CAP) isolated from porcine heart and vasoactive intestinal peptide (VIP) on ion transport were investigated in the winter flounder intestine. Partially purified CAP caused a two- to sixfold increase in the serosa-negative short-circuit current (Isc) with no significant change in tissue conductance. CAP significantly inhibited the serosal-to-mucosal (S-M) unidirectional Cl flux without affecting either Na or Rb transepithelial fluxes. The Isc after the addition of CAP was completely inhibited by 0.1 microM atriopeptin III (AP-3), 10 microM bumetanide, and 100 microM 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP). In contrast to the effects of CAP on Isc, VIP decreased the serosa-negative Isc by 40-60%. VIP stimulated the S-M unidirectional Cl flux without affecting transepithelial Na transport. When food was present in the intestine, the basal Isc was occasionally found to be serosa positive, ranging between 10 and 40 microA/cm2. Treatment of tissues exhibiting serosa-positive currents with VIP resulted in an increase (positive direction) in Isc. Addition of CAP to tissues with a serosa-positive Isc or to tissues pretreated with VIP resulted in a serosa-negative Isc.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Protease-activated receptor-1 stimulates Ca(2+)-dependent Cl(-) secretion in human intestinal epithelial cells.

The thrombin receptor, protease-activated receptor-1 (PAR-1), has wide tissue distribution and is involved in many physiological functions. Because thrombin is in the intestinal lumen and mucosa during inflammation, we sought to determine PAR-1 expression and function in human intestinal epithelial cells. RT-PCR showed PAR-1 mRNA expression in SCBN cells, a nontransformed duodenal epithelial cell line. Confluent SCBN monolayers mounted in Ussing chambers responded to PAR-1 activation with a Cl(-)-dependent increase in short-circuit current. The secretory effect was blocked by BaCl2 and the Ca(2+)-ATPase inhibitor thapsigargin, but not by the L-type Ca(2+) channel blocker verapamil or DIDS, the nonselective inhibitor of Ca(2+)-dependent Cl(-) transport. Responses to thrombin and PAR-1-activating peptides exhibited auto- and crossdesensitization. Fura 2-loaded SCBN cells had increased fluorescence after PAR-1 activation, indicating increased intracellular Ca(2+). RT-PCR showed that SCBN cells expressed mRNA for the cystic fibrosis transmembrane conductance regulator (CFTR) and hypotonicity-activated Cl(-) channel-2 but not for the Ca(2+)-dependent Cl(-) channel-1. PAR-1 activation failed to increase intracellular cAMP, suggesting that the CFTR channel is not involved in the Cl(-) secretory response. Our data demonstrate that PAR-1 is expressed on human intestinal epithelial cells and regulates a novel Ca(2+)-dependent Cl(-) secretory pathway. This may be of clinical significance in inflammatory intestinal diseases with elevated thrombin levels.

Calcium↗
PubMed1987

Inhibitory effect of somatostatin on cholera toxin-induced diarrhea and glycoenzyme secretion in rat intestine.

The effects of somatostatin on cholera toxin-induced secretory diarrhea and the appearance of glycoenzymes in the intestinal lumen and intestinal lymph were investigated in rat small intestine. After exposure to cholera toxin, marked fluid accumulation in the small intestinal tract and elevation of the jejunal mucosal cyclic AMP (cAMP) concentration were observed. The activity of alkaline phosphatase, aminopeptidase and sucrase increased in the intestinal lumen after toxin exposure. In intestinal lymph, alkaline phosphatase activity was increased after cholera toxin administration, while aminopeptidase activity remained unchanged. Somatostatin suppressed cholera toxin-induced secretory diarrhea, but it did not affect the elevated mucosal cAMP concentration. This peptide also inhibited the appearance of glycoenzymes in the intestinal lumen and lymph induced by cholera toxin administration. These results suggest that somatostatin exerts its inhibitory effects on cholera toxin-induced secretory diarrhea and on the appearance of glycoenzymes in the intestinal lumen and lymph by affecting processes beyond cAMP formation.

Alkaline Phosphatase↗
PubMed2002

Vasoactive intestinal polypeptide-secreting tumor (VIPoma) with liver metastases: dramatic and durable symptomatic benefit from hepatic artery embolization, a case report.

Neuroendocrine tumors often manifest an excess production of hormones that create severe metabolic abnormalities resulting in significant patient morbidity, independent of the tumor burden itself. VIPomas are rare neuroendocrine tumors arising from the pancreas and are associated with secretory diarrhea and electrolyte disturbances. We present a patient with VIPoma and hepatic metastases who had greater than 10 loose stools a day for 4 yr since diagnosis, despite debulking surgery, multiple antidiarrheal medications, large doses of octreotide, and targeted radioisotope injections. The patient required several hospitalizations for treatment of dehydration and electrolyte disturbances, despite receiving daily intravenous fluids at home. Hepatic artery embolization (HAE) immediately stopped the patient's diarrhea and provided a return to normal formed stools without any other symptom-support measures. One year after HAE, the patient remains asymptomatic and has returned to a productive life. HAE can be a very effective and durable treatment modality for patients with metastatic VIPomas (or other neuroendocrine tumors) and who are clinically symptomatic from the effects of hormone hypersecretion.

Antidiarrheals↗