In mice, 50% of linaclotide-induced fluid loss did not involve cGKII, despite dependence on CFTR activation and NHE3 inhibition.
In plain wordsIn mice, half of linaclotide-induced intestinal fluid loss did not involve cGKII.
- Peptide
- Linaclotide
- Outcome
- Not applicablecGKII-independent fluid loss
- Study
mousen: not reported in source
Perfused proximal jejunum in anesthetized mice- Outcome group
- Receptor activity and mechanism · Gastrointestinal
Source sentences
but 50% of the linaclotide-induced fluid loss in vivo, while dependent on CFTR activation and NHE3 inhibition, does not involve cGKII,
2 context sentences(design, population, supporting numbers)
we studied the effect of 10-7M of the STa analogue linaclotide on short circuit current (Isc) of chambered isolated jejunal mucosa, and on the in vivo action on fluid transport in a perfused segment of proximal jejunum of anesthetized mice.
The selected mice were deficient of transport (NHE3, CFTR, Slc26a3/a6), adaptor (NHERF1-3), or signal transduction molecules [cGMP-dependent kinase II (GKII)] considered to be downstream effectors after STa/linaclotide binding to guanylate cyclase C (GCC).
In this study, Linaclotide was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Linaclotide.