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Effects of endogenous cannabinoid anandamide on excitation-contraction coupling in rat ventricular myocytes.
Cell Calcium. 2014 Feb; 55(2):104-18.CC

Abstract

A role for anandamide (N-arachidonoyl ethanolamide; AEA), a major endocannabinoid, in the cardiovascular system in various pathological conditions has been reported in earlier reports. In the present study, the effects of AEA on contractility, Ca2+ signaling, and action potential (AP) characteristics were investigated in rat ventricular myocytes. Video edge detection was used to measure myocyte shortening. Intracellular Ca2+ was measured in cells loaded with the fluorescent indicator fura-2 AM. AEA (1 μM) caused a significant decrease in the amplitudes of electrically evoked myocyte shortening and Ca2+ transients. However, the amplitudes of caffeine-evoked Ca2+ transients and the rate of recovery of electrically evoked Ca2+ transients following caffeine application were not altered. Biochemical studies in sarcoplasmic reticulum (SR) vesicles from rat ventricles indicated that AEA affected Ca2+ -uptake and Ca2+ -ATPase activity in a biphasic manner. [3H]-ryanodine binding and passive Ca2+ release from SR vesicles were not altered by 10 μM AEA. Whole-cell patch-clamp technique was employed to investigate the effect of AEA on the characteristics of APs. AEA (1 μM) significantly decreased the duration of AP. The effect of AEA on myocyte shortening and AP characteristics was not altered in the presence of pertussis toxin (PTX, 2 μg/ml for 4 h), AM251 and SR141716 (cannabinoid type 1 receptor antagonists; 0.3 μM) or AM630 and SR 144528 (cannabinoid type 2 receptor antagonists; 0.3 μM). The results suggest that AEA depresses ventricular myocyte contractility by decreasing the action potential duration (APD) in a manner independent of CB1 and CB2 receptors.

Authors+Show Affiliations

Laboratory of Functional Lipidomics, Department of Pharmacology, College of Medicine and Health Sciences, UAE University, Al Ain, Abu Dhabi, United Arab Emirates.Bogomoletz Institute of Physiology and International Center of Molecular Physiology, National Academy of Sciences of Ukraine, Kyiv-24, Ukraine.Laboratory of Functional Lipidomics, Department of Pharmacology, College of Medicine and Health Sciences, UAE University, Al Ain, Abu Dhabi, United Arab Emirates.Department of Biochemistry, College of Medicine and Health Sciences, UAE University, Al Ain, Abu Dhabi, United Arab Emirates.Department of Biological Sciences, Schmid College of Science and Engineering, Chapman University, One University Drive, Orange, CA 92866, USA.Department of Physiology, College of Medicine and Health Sciences, UAE University, Al Ain, Abu Dhabi, United Arab Emirates.Bogomoletz Institute of Physiology and International Center of Molecular Physiology, National Academy of Sciences of Ukraine, Kyiv-24, Ukraine.Laboratory of Functional Lipidomics, Department of Pharmacology, College of Medicine and Health Sciences, UAE University, Al Ain, Abu Dhabi, United Arab Emirates. Electronic address: murat_oz@uaeu.ac.ae.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24472666

Citation

Al Kury, Lina T., et al. "Effects of Endogenous Cannabinoid Anandamide On Excitation-contraction Coupling in Rat Ventricular Myocytes." Cell Calcium, vol. 55, no. 2, 2014, pp. 104-18.
Al Kury LT, Voitychuk OI, Ali RM, et al. Effects of endogenous cannabinoid anandamide on excitation-contraction coupling in rat ventricular myocytes. Cell Calcium. 2014;55(2):104-18.
Al Kury, L. T., Voitychuk, O. I., Ali, R. M., Galadari, S., Yang, K. H., Howarth, F. C., Shuba, Y. M., & Oz, M. (2014). Effects of endogenous cannabinoid anandamide on excitation-contraction coupling in rat ventricular myocytes. Cell Calcium, 55(2), 104-18. https://doi.org/10.1016/j.ceca.2013.12.005
Al Kury LT, et al. Effects of Endogenous Cannabinoid Anandamide On Excitation-contraction Coupling in Rat Ventricular Myocytes. Cell Calcium. 2014;55(2):104-18. PubMed PMID: 24472666.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of endogenous cannabinoid anandamide on excitation-contraction coupling in rat ventricular myocytes. AU - Al Kury,Lina T, AU - Voitychuk,Oleg I, AU - Ali,Ramiz M, AU - Galadari,Sehamuddin, AU - Yang,Keun-Hang Susan, AU - Howarth,Frank Christopher, AU - Shuba,Yaroslav M, AU - Oz,Murat, Y1 - 2014/01/05/ PY - 2013/09/19/received PY - 2013/11/25/revised PY - 2013/12/26/accepted PY - 2014/1/30/entrez PY - 2014/1/30/pubmed PY - 2014/9/30/medline KW - Anandamide KW - Contraction KW - Endocannabinoid KW - Intracellular calcium KW - Ventricular action potential KW - Ventricular myocytes SP - 104 EP - 18 JF - Cell calcium JO - Cell Calcium VL - 55 IS - 2 N2 - A role for anandamide (N-arachidonoyl ethanolamide; AEA), a major endocannabinoid, in the cardiovascular system in various pathological conditions has been reported in earlier reports. In the present study, the effects of AEA on contractility, Ca2+ signaling, and action potential (AP) characteristics were investigated in rat ventricular myocytes. Video edge detection was used to measure myocyte shortening. Intracellular Ca2+ was measured in cells loaded with the fluorescent indicator fura-2 AM. AEA (1 μM) caused a significant decrease in the amplitudes of electrically evoked myocyte shortening and Ca2+ transients. However, the amplitudes of caffeine-evoked Ca2+ transients and the rate of recovery of electrically evoked Ca2+ transients following caffeine application were not altered. Biochemical studies in sarcoplasmic reticulum (SR) vesicles from rat ventricles indicated that AEA affected Ca2+ -uptake and Ca2+ -ATPase activity in a biphasic manner. [3H]-ryanodine binding and passive Ca2+ release from SR vesicles were not altered by 10 μM AEA. Whole-cell patch-clamp technique was employed to investigate the effect of AEA on the characteristics of APs. AEA (1 μM) significantly decreased the duration of AP. The effect of AEA on myocyte shortening and AP characteristics was not altered in the presence of pertussis toxin (PTX, 2 μg/ml for 4 h), AM251 and SR141716 (cannabinoid type 1 receptor antagonists; 0.3 μM) or AM630 and SR 144528 (cannabinoid type 2 receptor antagonists; 0.3 μM). The results suggest that AEA depresses ventricular myocyte contractility by decreasing the action potential duration (APD) in a manner independent of CB1 and CB2 receptors. SN - 1532-1991 UR - https://www.unboundmedicine.com/medline/citation/24472666/Effects_of_endogenous_cannabinoid_anandamide_on_excitation_contraction_coupling_in_rat_ventricular_myocytes_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0143-4160(13)00158-9 DB - PRIME DP - Unbound Medicine ER -