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EFFECTS OF DIADENOSINE POLYPHOSPHATES ON INWARD RECTIFIER POTASSIUM CURRENTS IN RAT CARDIOMYOCYTES

Abstract

Diadenosine polyphosphates are now considered as a novel class of endogenous paracrine signal compounds. The putative role of these compounds in pathogenesis of myocardial infarction was proposed, since the concentration of diadenosine polyphosphates increases in the cardiac tissue following the ischemic lesion and myocardial necrosis. Therefore, possible effects of diadenosine polyphosphates on cardiac electrical activity and their ionic mechanisms are of considerable interest. In the present study we have investigated the effects of diadenosine pentaphosphate (Ap5A), diadenosine tetraphosphate (Ap4A) and NAD+ on transmembrae currents, belonging to the family of potassium inward rectifiers: background inward rectifier (IK1), ATP-dependent potassium current (IKATP) and acetylcholine-dependent current (IKACh). Experiments were performed using the whole-cell patch-clamp technique on isolated atrial and ventricular rat cardiomyocytes. We have demonstrated that none of tested adenine compounds affects IK1 and IKACh. Ap5A (10–5М) induces considerable decrease of both inward and outward component of IKATP by 22,1 and 19% of control value, respectively. Higher concentration of Ap5A (3×10–5М) produces stronger suppression of IKATP — by 47,5 and 37,8%, respectively. However, IKATP turned out to be insensitive to Ap4A and NAD+.

About the Authors

D. V. Abramochkin
кафедры физиологии человека и животных биологического факультета МГУ
Russian Federation


K. B. Pustovit
кафедры физиологии человека и животных биологического факультета МГУ
Russian Federation


T. S. Filatova
кафедры физиологии человека и животных биологического факультета МГУ
Russian Federation


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Review

For citations:


Abramochkin D.V., Pustovit K.B., Filatova T.S. EFFECTS OF DIADENOSINE POLYPHOSPHATES ON INWARD RECTIFIER POTASSIUM CURRENTS IN RAT CARDIOMYOCYTES. Vestnik Moskovskogo universiteta. Seriya 16. Biologiya. 2015;(4):3-7. (In Russ.)

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ISSN 0137-0952 (Print)