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Muscarinic receptor subtypes in the alimentary tract

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Tobin G., Giglio D., Lundgren O.
Journal of Physiology and Pharmacology
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2009
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tom 60
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nr 1
3-21
Acetylcholine is a transmitter in preganglionic autonomic and postganglionic parasympathetic nerves and a non-neuronal paracrine mediator in the alimentary tract. Acetylcholine is involved in the control of almost any function within these organ systems, and almost every cell type expresses multiple muscarinic receptor subtypes. Although muscarinic receptors at non-neuronal effector cells commonly are of the M3 subtype, the population usually consists of a mixture of muscarinic receptor subtypes often co-acting postsynaptically. However, the pattern of heterogeneity of varies between different tissues. The population in gland parenchymal tissue often consists of a mixture of M1 and M3 receptors, smooth muscle tissue of the gut of M2 and M3, blood vessels of M1, M3, M4 and M5 and neuronal cells of M1 and M4. Nitric oxide production, effects on inflammation and proliferation may involve M1, M3 and M5 receptors. Muscarinic receptors expressed on nerve terminals may indirectly modulate the responses by inhibition or facilitation of neuronal transmission in the autonomic nervous system. The present review describes signalling mechanisms, expression and functional effects of muscarinic receptors in salivary glands and in the gastrointestinal tract.
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Time-dependent model to mimic acetylcholine induced vasodilatation in arterial smooth muscle cells

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Sahrawat T. R., Chatterjee D.
International Letters of Natural Sciences
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2016
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tom 52
Computational approaches for spatial modeling of dynamics of the intercellular distribution of molecules can parse, simplify, classify and organize the spatiotemporal richness of any biochemical pathway and demonstrate its impact on the cells function by simply coupling it with the downstream effecters. One such online system biology modeling package is Virtual cell that provides a unique open source software and it’s used for making mathematical models to simulate the cytoplasmic control of molecule that interact to produce certain cellular behavior. In our present study, a spatial model for time dependent acetylcholine induced relaxation of vascular endothelial cells lining the lumen of blood vessel that regulate the contractility of the arteries was generated. The time-dependent action of neurotransmitter acetylcholine for total time period for 1 second was studied on the endothelial cell at an interval of every 0.05 seconds. Such time simulated spatial models may be useful for testing and developing new hypotheses, interpretation of results and understand the dynamic behavior of cells.
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Clonidine-induced coronary vasodilatation in isolated guinea pig heart is not mediated by endothelial alpha2 adrenoceptors

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Chlopicki S., Kozlovski V. I., Gryglewski R. J.
Journal of Physiology and Pharmacology
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2003
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tom 54
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nr 4
Functional role of endothelial alpha2-adrenoceptor in coronary circulation remains unclear. Clonidine, an agonist of alpha2-adrenoceptors, was reported to induce coronary vasodilatation via stimulation of endothelial alpha2-adrenoceptors or coronary vasoconstriction involving vascular smooth muscle alpha2-adrenoceptors. Moreover, H2 receptor-dependent responses to clonidine were described. Here, we reassess the contribution of endothelial alpha2-adrenoceptor and H2 receptors to coronary flow and contractility responses induced by clonidine in the isolated guinea pig heart. We found that clonidine (10-9 - 10-6 M) produced concentration-dependent coronary vasoconstriction without a significant change in contractility. This response was inhibited by the alpha1/alpha2-adrenoceptor antagonist - phentolamine (10-5 M) and the selective alpha2-adrenoceptor antagonist yohimbine (10-6 M), but it was not changed by the selective alpha1-adrenoceptor antagonist prazosin (10-6 M). In the presence of nitric oxide synthase inhibitor, L-NAME (10-4 M) the clonidine-induced vasoconstriction was potentiated. Clonidine at high concentrations of 10-5 – 3 x 10-5 M produced coronary vasodilatation, and an increase in myocardial contractility. These responses were abolished by a selective H2-receptor antagonist, ranitidine (10-5 M), but not by phentolamine (10-5 M). We conclude that in the isolated guinea pig heart, clonidine-induced vasoconstriction is mediated by activation of smooth muscle alpha2-adrenoceptors whereas clonidine-induced coronary vasodilatation is mediated by activation of vascular H2 histaminergic receptors. Accordingly, endothelial alpha2-adrenoceptors does not seem to play a major role in coronary flow response induced by clonidine.
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