EFFECT OF EXERCISE AND CHRONIC ADMINISTRATION OF NANDROLONE DECANOATE ON EXPRESSION OF RAT HEART SARCOLEMMAL ATP- SENSITIVE POTASSIUM CHANNELS

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BAYAT GH.; HAJIZADEH S.; SAFARI F.; GOUDARZVAND M.; SHOKRI S.; POURKHALILI KH.; ALAVIAN F.

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Journal Paper

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Journal: Feyz Medical Sciences Journal Year:2012 | Volume:16 | Issue:2 (SERIAL 62) Page(s): 102-111

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Title

EFFECT OF EXERCISE AND CHRONIC ADMINISTRATION OF NANDROLONE DECANOATE ON EXPRESSION OF RAT HEART SARCOLEMMAL ATP- SENSITIVE POTASSIUM CHANNELS

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Keywords

EXERCISE

NANDROLONE DECANOATE

KATP SENSITIVE POTASSIUM CHANNELS

RAT HEART

Abstract

Background: The anabolic androgenic steroids are known to stimulate muscle protein synthesis and hypertrophy. Cardiomyocytes have two types of ATP-sensitive potassium channels in sarcolemma (sarcKATP) and in mitochondria (mitKATP). Activation of the sarcKATP channels has been proposed to protect against ischemia-reperfusion injury. This study aimed to investigate the effect of NANDROLONE DECANOATE (ND) on the expression of sarcKATP channels in the presence and absence of EXERCISE in RAT HEART.Materials and Methods: In this experimental study, 40 adult male rats were divided into five groups: control, vehicle, ND, EXERCISE and EXERCISE- ND group. Rats in the EXERCISE group were submitted to a running program on a treadmill, 5 days a week for 10 weeks. In addition, rats in the ND and EXERCISE- ND groups received a weekly intramuscular injection of ND (10 mg/kg) for 10 weeks. Expression of the KATP channel subunits (Kir 6.2 and SUR2) was determined using the Western blotting method.Results: ND administration had no effect on the expression of sarcKATP channel subunits in the sedentary group, while the chronic EXERCISE significantly increased the expression of KATP channel subunits (P=0.01). Moreover, the ND administration significantly decreased the Kir 6.2 (P=0.001) and SUR2 (P=0.05) subunits in the EXERCISEd animals.Conclusion: Chronic EXERCISE increases the expression of sarcKATP channels and the NDinduced expression decrement of the channels is probably one of the mechanisms involved in the impairment of EXERCISE- induced cardioprotection in RAT HEART.

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