Carnitine modulates crucial myocardial adenosine triphosphatases and acetylcholinesterase enzyme activities in choline-deprived rats

Author:

Strilakou Athina A.1,Tsakiris Stylianos T.2,Kalafatakis Konstantinos G.2,Stylianaki Aikaterini T.1,Karkalousos Petros L.3,Koulouris Andreas V.1,Mourouzis Iordanis S.1,Liapi Charis A.1

Affiliation:

1. Department of Pharmacology, Medical School, National and Kapodistrian University of Athens, 75 Mikras Asias Street, Athens GR-11527, Greece.

2. Laboratory of Physiology, Medical School, National and Kapodistrian University of Athens, Athens, Greece.

3. Department of Medical Laboratories, Technological Institute of Athens, Athens, Greece.

Abstract

Choline is an essential nutrient, and choline deficiency has been associated with cardiovascular morbidity. Choline is also the precursor of acetylcholine (cholinergic component of the heart’s autonomic nervous system), whose levels are regulated by acetylcholinesterase (AChE). Cardiac contraction–relaxation cycles depend on ion gradients established by pumps like the adenosine triphosphatases (ATPases) Na+/K+-ATPase and Mg2+-ATPase. This study aimed to investigate the impact of dietary choline deprivation on the activity of rat myocardial AChE (cholinergic marker), Na+/K+-ATPase, and Mg2+-ATPase, and the possible effects of carnitine supplementation (carnitine, structurally relevant to choline, is used as an adjunct in treating cardiac diseases). Adult male albino Wistar rats were distributed among 4 groups, and were fed a standard or choline-deficient diet for one month with or without carnitine in their drinking water (0.15% w/v). The enzyme activities were determined spectrophotometrically in the myocardium homogenate. Choline deficiency seems to affect the activity of the aforementioned parameters, but only the combination of choline deprivation and carnitine supplementation increased myocardial Na+/K+-ATPase activity along with a concomitant decrease in the activities of Mg2+-ATPase and AChE. The results suggest that carnitine, in the setting of choline deficiency, modulates cholinergic myocardial neurotransmission and the ATPase activity in favour of cardiac work efficiency.

Publisher

Canadian Science Publishing

Subject

Physiology (medical),Pharmacology,General Medicine,Physiology

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