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• W2017651674 abstract "In normal intestine, cyclic nucleotides (adenosine 3',5'-cyclic monophosphate [cAMP], guanosine 3',5'-cyclic monophosphate) and Ca(2+) inhibit neutral sodium absorption. In contrast, in the jejunum of a knockout mouse model of cystic fibrosis (CF), agents that elevate intracellular cAMP levels did not inhibit neutral sodium absorption, suggesting that the antiabsorptive effect of cAMP is dependent on the cystic fibrosis transmembrane conductance regulator (CFTR). The aim of the present study was to determine if a prostaglandin E(1) analogue, which causes elevation of intracellular cAMP and Ca(2+) levels, inhibits neutral sodium absorption in patients with CF in vivo.Electrolyte and water absorption/secretion was measured during steady state perfusion of the jejunum with a balanced electrolyte solution. Patients with CF and healthy subjects were studied under basal conditions and during intraluminal infusion of a prostaglandin E(1) analogue (misoprostol).The rate of neutral sodium absorption in the basal state was similar in healthy subjects and patients with CF. Prostaglandin infusion markedly reduced neutral sodium absorption in both healthy subjects and patients with CF. Prostaglandin caused high rates of electrolyte and water secretion in healthy subjects but only trivial rates of secretion in patients with CF.CFTR mutations causing CF in humans do not prevent prostaglandin E(1) inhibition of neutral sodium absorption, even though these mutations produce a severe defect in prostaglandin-stimulated electrolyte secretion. These findings suggest that an intact antiabsorptive response to either cAMP or Ca(2+) may contribute to the relatively low level of intestinal disease in patients with CF." @default.
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• W2017651674 date "2004-07-01" @default.
• W2017651674 modified "2023-09-26" @default.
• W2017651674 title "Inhibition of neutral sodium absorption by a prostaglandin analogue in patients with cystic fibrosis" @default.
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• W2017651674 doi "https://doi.org/10.1053/j.gastro.2004.03.064" @default.
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