ATP-sensitive K+-channel

ATP-sensitive K+ channel ATP-regulated K+ channel Kaxp channel SURx/Kir6.x channel... 

Abndnla R, Matchkov W, Jeppesen PB, Nilsson H, AaUejaer C, Hermansen K. (2008) Rebandioside A directly stimnlates insulin secretion from pancreatic beta cells A glucose-dependent action via inhibition of ATP-sensitive K-channels. Diabetes ObesMetab 10 1074-1085. 

Tang and colleagues proposed that HA increases ATP-sensitive K+ channel currents, which may underlie the observed HA vasorelaxation, and suggested that enhanced production of free radicals is involved in this physiological response. These results are consistent with the observations of Huang, who suggested that HA-induced relaxation of... 

Miki TK et al. The structure and function of the ATP-sensitive K+ channel in insulin-secreting pancreatic beta-cells. J Molec Endocrinol 1999 22 113-123. 

Glucotrol (Glipizide) 10.7 (0.5) 14.1 (0.5) 13.1 (0.6) A second generation sulfonylurea that blocks ATP-sensitive K-channels in the membrane of beta cells, stimulating the release of insulin. 

Gross GJ, Fryer RM. (1999) Sarcolemmal versus mitochondrial ATP-sensitive K channels and myocardial preconditioning. Circ Res 84, 973-9. 

ATP sensitive K channels. They lower down the blood sugar level in type 11 diabetics and non-diabetic individuals. They also decrease the elevated plasma free fatty acid levels. They also sensitize the target tissues to action of insulin by increasing the number of insulin receptors. 

Ocana, M. and Baeyens, J. M. Role of ATP-sensitive K channels in antinociception induced by R-PIA, an adenosine A1 receptor agonist, Naunyn-Schmiedeberg s Archiv of Pharmacology 1994, 350, 57-62. 

Ocana, M., Del Pozo, E., Barrios, M., Baeyens, J. M. Subgroups among p-opioid receptor agonists distinguished by ATP-sensitive K+ channel-acting drugs, British Journal of Pharmacology 1995, 114, 1296-1302. 

NIDDM is strongly associated with obesity,dd and dieting and exercise often provide adequate control of blood glucose. Sulfonylurea drugs such as the following induce an increase in the number of insulin receptors formed and are also widely used in treatment of the condition.66 These drugs bind to and inhibit ATP-sensitive K+ channels in the P cell membranes. A defect in this sulfonylurea receptor has been associated with excessive insulin secretion... 

The absorption of sulfonylureas from the upper gastrointestinal tract is fairly rapid and complete. The agents are transported in the blood as protein-bound complexes. As they are released from protein-binding sites, the free (unbound) form becomes available for diffusion into tissues and to sites of action. Specific receptors are present on pancreatic islet p-cell surfaces which bind sulfonylureas with high affinity. Binding of sulfonylureas to these receptors appears to be coupled to an ATP-sensitive K+ channel to stimulate insulin secretion. These agents may also potentiate insulin-stimulated glucose transport in adipose tissue and skeletal muscle. 

Ashcroft FM, Gribble FM. ATP-sensitive K+ channels and insulin secretion their role in health and disease. Diabetologia 1999 42(8) 903-19. 

Saraya A, Yokokura M, Gonoi T, Seino S. Effects of fluoroquinolones on insulin secretion and betacell ATP-sensitive K+ channels. Eur J Pharmacol... 

Genistein (42) was found to affect many other types of channels, but the main proposed mechanism of these interactions was indirect. In most cases a PTK pathway was suggested as a putative explanation of the observed effects. Since genistein (42) is a well-known inhibitor of this kinase, we will not focus on those papers and only a short list will be presented. Such a mechanism was mentioned in the case of inhibition of ATP-sensitive K+ channels [325], cardiac slowly activating delayed-rectifier K+ current [326], L-type calcium channels [327,328] (contrary to the direct interaction proposed by Chiang et al. [306] and Yokoshiki et al. [307]), P/Q-type calcium channels in rat hippocampal neurons [329], and carotid baroreceptor activity [330]. A PTK-dependent mechanism was also proposed as the explanation of potentiation of neuronal a7 nAGhRs by genistein (42) [331]. 

The spinal antinociceptive effect of DPDPE is blocked totally by a small conductance Ca2 + -activated K + channel blocker apamin [109]. The DPDPE-induced spinal antinociception is not inhibited by a ATP-sensitive K + channel blocker glyburide [109], Like morphine, tetraethylammonium, 4-aminopyridine, and charybdotoxin are unable to block the effects of DPDPE [109], These findings suggest that the modulation of apamin-sensitive K + channels appears to play a role in the DPDPE-induced antinociception in the spinal cord. 

ASPPR, aspartate protease ATP, adenosine 5 -triphosphate 5 -ATP, adenosine 5 -triphosphate ATP-K+ CH, ATP-sensitive K+ channel ATP-R, ATP receptor autophos n, autophosphorylation... 

Elevation in the ATP/ADP ratio induces closure of cell-surface ATP-sensitive K+ channels, leading to cell-membrane depolarisation. 

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