Agnieszka Polak1, Ewa Harasim-Symbor2, Barbara Malinowska3, Irena Kasacka4, Anna Pędzińska-Betiuk3, Jolanta Weresa3, Adrian Chabowski1. 1. Department of Physiology, Medical University of Bialystok, Bialystok, Poland. 2. Department of Physiology, Medical University of Bialystok, Bialystok, Poland. Electronic address: eharasim@umb.edu.pl. 3. Department of Experimental Physiology and Pathophysiology, Medical University of Białystok, Białystok, Poland. 4. Department of Histology and Cytophysiology, Medical University of Białystok, Białystok, Poland.
Abstract
AIMS: There is significant evidence that the endocannabinoid system (ECS) takes part in the regulation of the cardiovascular system in hypertension. It is quite well established that hypertension causes several changes in the heart metabolism, but it is still unknown whether the ECS affects this process. Therefore, we investigated the influence of prolonged ECS activation on myocardial lipid metabolism in deoxycorticosterone acetate (DOCA)-salt hypertensive rats by chronic fatty acid amide hydrolase (FAAH) inhibition. MATERIALS AND METHODS: We examined the uptake and oxidation of palmitic acid during the heart perfusion as well as intramyocardial and plasma lipid contents using gas liquid chromatography. Total, plasmalemmal and intracellular expressions of selected proteins were estimated by the Western blot technique. Moreover, the left ventricle's morphology, including myocardial vessels density, was measured using immunohistochemistry. KEY FINDINGS: We demonstrated that hypertension induced cardiomyocytes and myocardial blood vessels hypertrophy, followed by a reduction in myocardial palmitate oxidation. Interestingly, prolonged activation of the ECS in the normotensive rats induced cardiomyocyte enlargement and intensified fatty acids metabolism. We have also shown that FAAH inhibition improved morphology of coronary blood vessels and only partially maintained its effect on lipid metabolism in the DOCA-salt hearts (i.e. elevated plasma and intramyocardial TAG contents as well as plasmalemmal FAT/CD36 and total FATP1 expressions). SIGNIFICANCE: This study revealed that chronic FAAH inhibition has no protective effects on the heart lipid metabolism in hypertension.
AIMS: There is significant evidence that the endocannabinoid system (ECS) takes part in the regulation of the cardiovascular system in hypertension. It is quite well established that hypertension causes several changes in the heart metabolism, but it is still unknown whether the ECS affects this process. Therefore, we investigated the influence of prolonged ECS activation on myocardial lipid metabolism in deoxycorticosterone acetate (DOCA)-salthypertensiverats by chronic fatty acid amide hydrolase (FAAH) inhibition. MATERIALS AND METHODS: We examined the uptake and oxidation of palmitic acid during the heart perfusion as well as intramyocardial and plasma lipid contents using gas liquid chromatography. Total, plasmalemmal and intracellular expressions of selected proteins were estimated by the Western blot technique. Moreover, the left ventricle's morphology, including myocardial vessels density, was measured using immunohistochemistry. KEY FINDINGS: We demonstrated that hypertension induced cardiomyocytes and myocardial blood vessels hypertrophy, followed by a reduction in myocardial palmitate oxidation. Interestingly, prolonged activation of the ECS in the normotensive rats induced cardiomyocyte enlargement and intensified fatty acids metabolism. We have also shown that FAAH inhibition improved morphology of coronary blood vessels and only partially maintained its effect on lipid metabolism in the DOCA-salt hearts (i.e. elevated plasma and intramyocardial TAG contents as well as plasmalemmal FAT/CD36 and total FATP1 expressions). SIGNIFICANCE: This study revealed that chronic FAAH inhibition has no protective effects on the heart lipid metabolism in hypertension.