ArticleBritish journal of pharmacology1999
Block of human aorta Kir6.1 by the vascular KATP channel inhibitor U37883A.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 26 citations in OpenAlex.
- The Pharmacology of ATP-Sensitive KHandbook of experimental pharmacology · 2021Article
- Electrophysiologic consequences of KATP gain of function in the heart: Conduction abnormalities in Cantu syndrome.Heart rhythm · 2015Article
- Label-free cell phenotypic profiling decodes the composition and signaling of an endogenous ATP-sensitive potassium channel.Scientific reports · 2014Article
- K(ATP) channel expression and pharmacological in vivo and in vitro studies of the K(ATP) channel blocker PNU-37883A in rat middle meningeal arteries.British journal of pharmacology · 2008Article
- The pore-forming subunit of the K(ATP) channel is an important molecular target for LPS-induced vascular hyporeactivity in vitro.British journal of pharmacology · 2005Article
- Molecular analysis of the subtype-selective inhibition of cloned KATP channels by PNU-37883A.British journal of pharmacology · 2004Article
- Different molecular sites of action for the KATP channel inhibitors, PNU-99963 and PNU-37883A.British journal of pharmacology · 2003Article
- Pharmacology of human sulphonylurea receptor SUR1 and inward rectifier K(+) channel Kir6.2 combination expressed in HEK-293 cells.British journal of pharmacology · 2000Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. A human aorta cDNA library was screened at low stringency with a rat pancreatic Kir6.1 cDNA probe and a homologue of Kir6.1 (hKir6.1) was isolated and sequenced. 2. Metabolic poisoning of Xenopus laevis oocytes with sodium azide and application of the K+ channel opener drug diazoxide induced K+ channel currents in oocytes co-injected with cRNA for hKir6.1 and hamster sulphonylurea receptor (SUR1), but not in oocytes injected with water or cRNA for hKir6.1 or SUR1 alone. 3. K+ channel currents due to hKir6.1+SUR1 or mouse Kir6.2+SUR1 were strongly inhibited by 1 microM glibenclamide. K+-current carried by hKir6.1+SUR1 was inhibited by the putative vascular-selective KATP channel inhibitor U37883A (IC50 32 microM) whereas current carried by Kir6.2+SUR1 or Shaker K+ channels was unaffected. 4. The data support the hypothesis that hKir6.1 is a component of the vascular KATP channel, although the lower sensitivity of hKir6.1+SUR1 to U37883A compared with native vascular tissues suggests the need for another factor or subunit. Furthermore, the data suggest that pharmacology of KATP channels can be determined by the pore-forming subunit as well as the sulphonylurea receptor and point to a molecular basis for the pharmacological distinction between vascular and pancreatic/cardiac KATP channels.
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