ArticleProceedings of the National Academy of Sciences of the United States of America1993
ATP-modulated K+ channels sensitive to antidiabetic sulfonylureas are present in adenohypophysis and are involved in growth hormone release.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 67 citations in OpenAlex.
- Latest Insights into the Pathophysiology of Migraine: the ATP-Sensitive Potassium Channels.Current pain and headache reports · 2020Review
- ATP sensitive potassium channel openers: A new class of ocular hypotensive agents.Experimental eye research · 2017Review
- Effect of sulfonylureas administered centrally on the blood glucose level in immobilization stress model.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2015Article
- Neuroprotective role of ATP-sensitive potassium channels in cerebral ischemia.Acta pharmacologica Sinica · 2013Review
- Cloning of a pore-forming subunit of ATP-sensitive potassium channel from Clonorchis sinensis.The Korean journal of parasitology · 2003Article
- Article
- Abnormalities of pancreatic islets by targeted expression of a dominant-negative KATP channel.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Nephropathy and growth hormone deficiency in a patient with mitochondrial tRNA(Leu(UUR)) mutation.Journal of medical genetics · 1996Article
- Coexistence of two classes of glibenclamide-inhibitable ATP-regulated K+ channels in avian skeletal muscle.Pflugers Archiv : European journal of physiology · 1995Article
- ATP-sensitive K+ channels in the kidney.Naunyn-Schmiedeberg's archives of pharmacologyReview
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The adenohypophysis contains high-affinity binding sites for antidiabetic sulfonylureas that are specific blockers of ATP-sensitive K+ channels. The binding protein has a M(r) of 145,000 +/- 5000. The presence of ATP-sensitive K+ channels (26 pS) has been demonstrated by electrophysiological techniques. Intracellular perfusion of adenohypophysis cells with an ATP-free medium to activate ATP-sensitive K+ channels induces a large hyperpolarization (approximately 30 mV) that is antagonized by antidiabetic sulfonylureas. Diazoxide opens ATP-sensitive K+ channels in adenohypophysis cells as it does in pancreatic beta cells and also induces a hyperpolarization (approximately 30 mV) that is also suppressed by antidiabetic sulfonylureas. As in pancreatic beta cells, glucose and antidiabetic sulfonylureas depolarize the adenohypophysis cells and thereby indirectly increase Ca2+ influx through L-type Ca2+ channels. The K+ channel opener diazoxide has an opposite effect. Opening ATP-sensitive K+ channels inhibits growth hormone secretion and this inhibition is eliminated by antidiabetic sulfonylureas.
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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.