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Gut Liver. 2016 Nov 15;10(6):881-889. doi: 10.5009/gnl15414.

Potassium Channelopathies and Gastrointestinal Ulceration.

Author information

1
Department of Cellular and Molecular Physiology, Yale University, New Haven, CT, USA.
2
Department of Internal Medicine, Section of Nephrology, Yale University, New Haven, CT, USA.

Abstract

Potassium channels and transporters maintain potassium homeostasis and play significant roles in several different biological actions via potassium ion regulation. In previous decades, the key revelations that potassium channels and transporters are involved in the production of gastric acid and the regulation of secretion in the stomach have been recognized. Drugs used to treat peptic ulceration are often potassium transporter inhibitors. It has also been reported that potassium channels are involved in ulcerative colitis. Direct toxicity to the intestines from nonsteroidal anti-inflammatory drugs has been associated with altered potassium channel activities. Several reports have indicated that the long-term use of the antianginal drug Nicorandil, an adenosine triphosphate-sensitive potassium channel opener, increases the chances of ulceration and perforation from the oral to anal regions throughout the gastrointestinal (GI) tract. Several of these drug features provide further insights into the role of potassium channels in the occurrence of ulceration in the GI tract. The purpose of this review is to investigate whether potassium channelopathies are involved in the mechanisms responsible for ulceration that occurs throughout the GI tract.

KEYWORDS:

Gastrointestinal tract; H⁺/K⁺-ATPase; Potassium channels; Ulceration

PMID:
27784845
PMCID:
PMC5087926
DOI:
10.5009/gnl15414
[Indexed for MEDLINE]
Free PMC Article
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