Interaction of adrenergic and purinergic receptors in the regulation of rat myocardial contractility in postnatal ontogeny

Anikina, T. A.; Zverev, A. A.; Ситдиков, Ф. Г.; Anisimova, I. N.

doi:10.1134/s1062360413060027

Cited by 4 publications

(2 citation statements)

References 20 publications

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“…Эффекты в сердце, связанные с действием агонистов рецепторов Р2-типа, и, соответственно, активацией рецепторов Р2, также различны у животных разного возраста. Так, эндогенный агонист рецепторов Р2-типа АТФ оказывает наиболее сильное влияние на сократимость в желудочковом и предсердном миокарде крысы на 21-е сут постнатального развития [17,18]. Таким образом, данные предыдущих работ позволяли предполагать, что ДАТФ, как физиологически активное вещество, относящееся к группе пуриновых соединений, может оказывать различное влияние на работу сердца у крыс различного возраста.…”

Section: результаты и обсуждениеunclassified

Effects of Extracellular Diadenosine Tetraphosphate on Action Potentials in the Atrial and Ventricular Myocardium of the Rat Heart during Early Postnatal Ontogenesis

Pustovit

Потехина

Pakhomov

et al. 2017

Moscow Univ. Biol.Sci. Bull.

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Section: результаты и обсуждениеunclassified

Effects of Extracellular Diadenosine Tetraphosphate on Action Potentials in the Atrial and Ventricular Myocardium of the Rat Heart during Early Postnatal Ontogenesis

Pustovit

Потехина

Pakhomov

et al. 2017

Moscow Univ. Biol.Sci. Bull.

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“…β2-adrenoceptor coupled with P2Y receptors stimulates release of ATP, leading to Ca 2+ mobilization from intracellular stores [ 20 ]. To all that, combined administration of β-adrenergic and P2X receptors agonists to the heart increased its contractility [ 21 ]. Moreover, studies on a transgenic model with cardiac-restricted β 2 -adrenoceptor overexpression (β 2 -TG) showed β 2 -adrenoceptor/nicotinamide adenine dinucleotide phosphate (NADPH) oxidase/ROS/p38 MAPK signaling pathway that indicated superoxide production as central to the detrimental signaling of β 2 -adrenoceptors [ 22 , 23 ].…”

Section: Introductionmentioning

confidence: 99%

Ibogaine-Mediated ROS/Antioxidant Elevation in Isolated Rat Uterus Is β-Adrenergic Receptors and KATP Channels Mediated

et al. 2021

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Ibogaine effects are mediated by cellular receptors, ATP depletion followed by ROS production and antioxidant enzyme activity elevation in a dose and time dependent manner. Since the role of KATP channels and β-adrenoceptors in ROS cellular circuit was established here we explored their role in ibogaine pro-antioxidant effectiveness. Single dose of ibogaine (10 mg/L i.e., 28.8 μmol/L) was applied to isolated rat uterus (spontaneous and Ca2+-stimulated) and contractility and antioxidant enzymes activity were monitored during 4 h. Ibogaine increased amplitude and frequency of spontaneous active uteri immediately after addition that was prevented by propranolol (β1 and β2 adrenoceptors selective antagonists) and glibenclamide (KATP sensitive channels inhibitor; only frequency) pre-treatment. In Ca2+-stimulated uteri, ibogaine decreased both amplitude and frequency after 4 h. Pre-treatment with propranolol abolished ibogaine induced amplitude lowering, while glibenclamide had no effect. In both types of active uterus, ibogaine induced a decrease in SOD1 and an increase in CAT activity after 2 h. In Ca2+-stimulated uterus, there was also a decrease of SOD2 activity after 2 h. After 4 h, SOD1 activity returned to the baseline level, but GSH-Px activity increased. Pre-treatment with both propranolol and glibenclamide abolished observed changes of antioxidant enzymes activity suggesting that ibogaine pro-antioxidative effectiveness is β-adrenergic receptors and KATP channels mediated.

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Cardiac purinergic signalling in health and disease

Burnstock

Pelleg

2014

Purinergic Signalling

118

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This review is a historical account about purinergic signalling in the heart, for readers to see how ideas and understanding have changed as new experimental results were published. Initially, the focus is on the nervous control of the heart by ATP as a cotransmitter in sympathetic, parasympathetic, and sensory nerves, as well as in intracardiac neurons. Control of the heart by centers in the brain and vagal cardiovascular reflexes involving purines are also discussed. The actions of adenine nucleotides and nucleosides on cardiomyocytes, atrioventricular and sinoatrial nodes, cardiac fibroblasts, and coronary blood vessels are described. Cardiac release and degradation of ATP are also described. Finally, the involvement of purinergic signalling and its therapeutic potential in cardiac pathophysiology is reviewed, including acute and chronic heart failure, ischemia, infarction, arrhythmias, cardiomyopathy, syncope, hypertrophy, coronary artery disease, angina, diabetic cardiomyopathy, as well as heart transplantation and coronary bypass grafts.

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Interaction of adrenergic and purinergic receptors in the regulation of rat myocardial contractility in postnatal ontogeny

Cited by 4 publications

References 20 publications

Effects of Extracellular Diadenosine Tetraphosphate on Action Potentials in the Atrial and Ventricular Myocardium of the Rat Heart during Early Postnatal Ontogenesis

Effects of Extracellular Diadenosine Tetraphosphate on Action Potentials in the Atrial and Ventricular Myocardium of the Rat Heart during Early Postnatal Ontogenesis

Ibogaine-Mediated ROS/Antioxidant Elevation in Isolated Rat Uterus Is β-Adrenergic Receptors and KATP Channels Mediated

Cardiac purinergic signalling in health and disease

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