ArticleGut2003
Non-genomic regulation of intermediate conductance potassium channels by aldosterone in human colonic crypt cells.
Article in Gut, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Potassium channels in intestinal epithelial cells and their pharmacological modulation: a systematic review.American journal of physiology. Cell physiology · 2021Pooled it
- Enteroendocrine cell regulation of the gut-brain axis.Frontiers in neuroscience · 2023Review
- Pathophysiological role of ion channels and transporters in gastrointestinal mucosal diseases.Cellular and molecular life sciences : CMLS · 2021Review
- Calmodulin Antagonist W-7 Enhances Intermediate Conductance CaThe Journal of membrane biology · 2021Article
- Goblet cell LRRC26 regulates BK channel activation and protects against colitis in mice.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Parallel intermediate conductance KAmerican journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Calcium-sensing receptor regulates intestinal dipeptide absorption via CaPhysiological reports · 2020Article
- Colonic Potassium Absorption and Secretion in Health and Disease.Comprehensive Physiology · 2018Review
- Upregulation of basolateral small conductance potassium channels (KCNQ1/KCNE3) in ulcerative colitis.Biochemical and biophysical research communications · 2016Article
- Characteristics of Kcnn4 channels in the apical membranes of an intestinal epithelial cell line.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- Basolateral potassium (IKCa) channel inhibition prevents increased colonic permeability induced by chemical hypoxia.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- Silencing of the mineralocorticoid receptor by ribonucleic acid interference in transgenic rats disrupts endocrine homeostasis.Molecular endocrinology (Baltimore, Md.) · 2008Article
- Effects of chronic hypoxia on electrogenic transport and transport-related oxygen consumption in rat distal colon.Digestive diseases and sciences · 2008Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAldosterone has a rapid, non-genomic, inhibitory effect on macroscopic basolateral K(+) conductance in the human colon, reducing its capacity for Cl(-) secretion. The molecular identity of the K(+) channels constituting this aldosterone inhibitable K(+) conductance is unclear.
aimTo characterise the K(+) channel inhibited by aldosterone present in the basolateral membrane of human colonic crypt cells.
methodsCrypts were isolated from biopsies of healthy sigmoid colon obtained during colonoscopy. The effect of aldosterone on basolateral K(+) channels, and the possible involvement of Na(+):H(+) exchange, were studied by patch clamp techniques. Total RNA from isolated crypts was subjected to reverse transcriptase-polymerase chain reaction (RT-PCR) using primers specific to intermediate conductance K(+) channels (KCNN4) previously identified in other human tissues.
resultsIn cell attached patches, 1 nmol/l aldosterone significantly decreased the activity of intermediate conductance (27 pS) K(+) channels by 31%, 53%, and 54% after 1, 5 and 10, minutes, respectively. Increasing aldosterone concentration to 10 nmol/l produced a further 56% decrease in channel activity after five minutes. Aldosterone 1-10 nmol/l had no effect on channel activity in the presence of 20 micro mol/l ethylisopropylamiloride, an inhibitor of Na(+):H(+) exchange. RT-PCR identified KCNN4 mRNA, which is likely to encode the 27 pS K(+) channel inhibited by aldosterone.
conclusionIntermediate conductance K(+) channels (KCNN4) present in the basolateral membranes of human colonic crypt cells are a target for the non-genomic inhibitory effect of aldosterone, which involves stimulation of Na(+):H(+) exchange, thereby reducing the capacity of the colon for Cl(-) secretion.
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Registered trials
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