K ATP Channels and Cardiovascular Disease

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منابع مشابه

ATP-sensitive K channels and disease: from molecule to malady

Ashcroft FM. ATP-sensitive K channels and disease: from molecule to malady. Am J Physiol Endocrinol Metab 293: E880–E889, 2007. First published July 24, 2007; doi:10.1152/ajpendo.00348.2007.—This essay is based on a lecture given to the American Physiological Society in honor of Walter B. Cannon, an advocate of homeostasis. It focuses on the role of the ATP-sensitive potassium K (KATP) channel ...

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The role of ATP-dependent K+ channels in antinociception, tolerance and morphine dependence

  Tolerance and dependence are two main problems that have limited morphine administration as an analgesic drug and they might be as a result of changes in the number and affinity of receptors, dysfunction of adenylate cyclase, impaired coupling between activated µ receptor and K+ channels, and changes in the K+ and Ca2+ channels. There are several reports concerning the role of some of these...

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Cardiovascular ATP-sensitive potassium channels

Sulfonylurea drugs stimulate endogenous insulin secretion by blockade of ATP-sensitive potassium channels in pancreatic beta cells. These drugs are widely used in the treatment of type 2 diabetes. However, as ATP-sensitive potassium channels also exist in cardiomyocytes and coronary and peripheral arterial vascular smooth muscle cells, sulfonylurea drug usage in theory may cause unwanted cardio...

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K(ATP) channels and insulin secretion disorders.

ATP-sensitive potassium (K(ATP)) channels are inhibited by intracellular ATP and activated by ADP. Nutrient oxidation in beta-cells leads to a rise in [ATP]-to-[ADP] ratios, which in turn leads to reduced K(ATP) channel activity, depolarization, voltage-dependent Ca(2+) channel activation, Ca(2+) entry, and exocytosis. Persistent hyperinsulinemic hypoglycemia of infancy (HI) is a genetic disord...

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Tolerance for ATP-insensitive K(ATP) channels in transgenic mice.

To examine the role of sarcolemmal K(ATP) channels in cardiac function, we generated transgenic mice expressing GFP-tagged Kir6.2 subunits with reduced ATP sensitivity under control of the cardiac alpha-myosin heavy chain promoter. Four founder mice were isolated, and both founders and progeny were all apparently normal and fertile. Electrocardiograms from conscious animals also appeared normal...

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ژورنال

عنوان ژورنال: Circulation Research

سال: 2013

ISSN: 0009-7330,1524-4571

DOI: 10.1161/circresaha.112.300514