NDLI: Basolateral PAR-2 receptors mediate KCl secretion and inhibition of Na+ absorption in the mouse distal colon

Content Provider	PubMed Central
Author	Cuffe, John E. Bertog, Marko Sara, Velázquez-rocha Dery, Olivier Bunnett, Nigel Korbmacher, Christoph
Copyright Year	2002
Abstract	Proteinase-activated receptor-2 (PAR-2) may participate in epithelial ion transport regulation. Here we examined the effect of mouse activating peptide (mAP), a specific activator of PAR-2, on electrogenic transport of mouse distal colon using short-circuit current (I SC) measurements. Under steady-state conditions, apical application of amiloride (100 μ m ) revealed a positive I SC component of 74.3 ± 6.8 μA cm−2 indicating the presence of Na+ absorption, while apical Ba2+ (10 mm) identified a negative I SC component of 26.2 ± 1.8 μA cm−2 consistent with K+ secretion. Baseline Cl− secretion was minimal. Basolateral addition of 20 μm mAP produced a biphasic I SC response with an initial transient peak increase of 11.2 ± 0.9 μA cm−2, followed by a sustained fall to a level 31.2 ± 2.6 μA cm−2 (n = 43) below resting I SC. The peak response was due to Cl− secretion as it was preserved in the presence of amiloride but was largely reduced in the presence of basolateral bumetanide (20 μm) or in the absence of extracellular Cl−. The secondary decline of I SC was also attenuated by bumetanide and by Ba2+, indicating that it is partly due to a stimulation of K+ secretion. In addition, the amiloride-sensitive I SC was slightly reduced by mAP, suggesting that inhibition of Na+ absorption also contributes to the I SC decline. Expression of PAR-2 in mouse distal colon was confirmed using RT-PCR and immunocytochemistry. We conclude that functional basolateral PAR-2 is present in mouse distal colon and that its activation stimulates Cl− and K+ secretion while inhibiting baseline Na+ absorption.
Related Links	http://dx.doi.org/10.1113/jphysiol.2001.013159
Ending Page	222
Page Count	14
Starting Page	209
File Format	PDF
ISSN	00223751
e-ISSN	14697793
Journal	The Journal of Physiology
Issue Number	Pt 1
Volume Number	539
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2002-02-01
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Physiology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Sports Science

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