ArticleBritish journal of pharmacology1994
Augmentation by intracellular ATP of the delayed rectifier current independently of the glibenclamide-sensitive K-current in rabbit arterial myocytes.
Article in British journal of pharmacology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 21 citations in OpenAlex.
- Cellular localization of mitochondria contributes to Kv channel-mediated regulation of cellular excitability in pulmonary but not mesenteric circulation.American journal of physiology. Lung cellular and molecular physiology · 2009Article
- Mitochondria-dependent regulation of Kv currents in rat pulmonary artery smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2008Article
- Electrophysiological and functional effects of the KCNQ channel blocker XE991 on murine portal vein smooth muscle cells.British journal of pharmacology · 2005Article
- Kv2.1/Kv9.3, a novel ATP-dependent delayed-rectifier K+ channel in oxygen-sensitive pulmonary artery myocytes.The EMBO journal · 1997Article
- Properties of a novel K+ current that is active at resting potential in rabbit pulmonary artery smooth muscle cells.The Journal of physiology · 1996Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elevation of intracellular ATP levels by flash photolysis of caged ATP augmented the delayed rectifier K-current (IKDR) in rabbit pulmonary artery myocytes. The percentage augmentation was unaffected when IKDR was inactivated by 50% (holding potential -40 mV), although the magnitude of the ATP-induced current was substantially reduced. Inactivation of 90% IKDR (holding potential -20 mV) virtually abolished the ATP-dependent augmentation. We conclude that modulation of IKDR by ATP does not require conversion of the glibenclamide-sensitive K-current (IK(ATP)).
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.