Related Experiment Video
Updated: Jul 5, 2026

Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique
Published on: November 11, 2022
[Physiological properties and possible correction of adenosine triphosphate-sensitive potassium channel function]
Abstract:
Unique function of ATP-sensitive K channels (K(ATP)) is maintenance of interrelation between a metabolism and excitability of cells of various bodies and fabrics. In smooth muscle cells activation KP channels lead to vasodilatation, in beta-cells of a pancreas these channels play a role in interface of excitability of a membrane and secretion of insulin. Sulfonylurea drugs lowering a level of glucose in blood which use for treatment of a 2 type diabetes,--influence, contacting SUR 1 subunit and oppressing thus a K(ATP) current. It leads to membranes depolarisation, to Ca2+ entrance in cells and secretions of insulin. As opposed to this, diazoxide and pinacidil which reduce allocation of insulin, reduce arterial pressure, are specific K(ATP) activators. These preparations render therapeutic effects, stimulating K(ATP) and as consequence, limit increase of a level intracellular Ca2+ at depolarisation. At an ischemia of heart activation of K(ATP) channels reduces duration of potential of action, and it leads to reduction of Ca2+ entrance and renders cardio protective action. For last years significant successes in understanding of molecular mechanisms, determines K(ATP) channels activity, and in finding-out of their role in physiological and pathological processes are achieved. In this review of the literature the basic achievements in this area, and also problems which should be solved are considered.
Related Concept Videos
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers
G-Protein Gated Ion Channels
Sensory organs,...
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers
Ligand-Gated Ion Channel Receptor: Gating Mechanism
Heart Failure Drugs: Inotropic Agents

