scholarly journals Esophagus: serotoninerdgic regulation

Author(s):  
A. M. Puzikov

Introduction: Serotonin (5-hydroxytryptamine, 5-HT) is a regulatory neurotransmitter and a hormone in the CNS and hole organs, the esophagus including. It is known that serotonin, activating its own receptors, stimulates contractile activity of the esophageal muscles. However, role of different type receptors in the 5-HT induced contractile activity of the esophagus is insufficiently known.The aim: — to determine which type of 5-HT receptors mediate serotonin dependent contractile activity of the esophagus.Material and methods: This is a electromyography study of rat esophagus contractile activity under serotonin stimulation of 5-HT3,4 and 5-HT2,1 receptors separately modulated. The role of different serotonin receptors in the 5-HT induced contractile activity of the esophagus was evaluated by measuring the amplitude and frequency of the slow wave electromyogram (EMG) by the noninvasive microelectrodes imposed on the adventitial layer of the esophagus.Results: Administration of the 5-HT3,4 receptors inhibitors excluded caused by serotonin the increment of EMG activity of the contractile activity of the esophagus. Administration of the 5-HT1,2 receptors inhibitors blocked the serotonin enhanced EMG activity of the esophagus.Conclusion: Our results indicate that serotonin is the important player in the regulation of the rat's esophagus contractility; 5-HT enhancing effect on contraction of the esophageal smooth muscles is mediated through the activation of 5-HT1,2 receptors expressed on the smooth muscle cells, and by activation of 5-HT3,4 receptors expressed on the ganglion neurons.

1986 ◽  
Vol 60 (5) ◽  
pp. 1518-1523 ◽  
Author(s):  
S. H. Constable ◽  
R. J. Favier ◽  
J. O. Holloszy

Phosphorylase activation reverses during prolonged contractile activity. Our first experiment was designed to determine whether this loss of ability to activate phosphorylase by stimulation of muscle contraction persists following exercise. Phosphorylase activation by stimulation of muscle contraction was markedly inhibited in rats 25 min after exhausting exercise. To evaluate the role of glycogen depletion, we accelerated glycogen utilization by nicotinic acid administration. A large difference in muscle glycogen depletion during exercise of the same duration did not influence the blunting of phosphorylase activation. Phosphorylase activation by stimulation of contraction was more severely inhibited following prolonged exercise than after a shorter bout of exercise under conditions that resulted in the same degree of glycogen depletion. A large difference in muscle glycogen repletion during 90 min of recovery was not associated with a significant difference in the ability of muscle stimulation to activate phosphorylase, which was still significantly blunted. Phosphorylase activation by epinephrine was also markedly inhibited in muscle 25 min after strenuous exercise but had recovered completely in glycogen-repleted muscle 90 min after exercise. These results provide evidence that an effect of exercise other than glycogen depletion is involved in causing the inhibition of phosphorylase activation; however, they do not rule out the possibility that glycogen depletion also plays a role in this process.


2009 ◽  
Vol 8 (4) ◽  
pp. 41-46
Author(s):  
I. V. Kovalyev ◽  
S. V. Gusakova ◽  
O. S. Melnik ◽  
M. B. Baskakov ◽  
L. V. Kapilevich ◽  
...  

The influence of of hydrogen peroxide on the contractile reactions of smooth muscle cells caused by hyperpotassium solution end phenylephrine in modulation a potassium conductance the membrane and the state of cytoskeleton elements has been investigated by the mechanographical method. It has multidirectional influence of hydrogen peroxide in the reduction of smooth muscles of rat aorta with the membrane depolarization hyperpotassium solution and action phenylephrine: phenylephrine decline in value and increase strength hyperpotassium contractures. We show that the cytoskeleton components involved in the mechanisms of action of hydrogen peroxide in the contractile reactions of smooth muscles of rat aorta caused by phenylephrine.


2016 ◽  
Vol 97 (1) ◽  
pp. 89-94 ◽  
Author(s):  
D S Sveshnikov ◽  
A V Kuchuk ◽  
V M Smirnov ◽  
G V Cherepanova

Review is devoted to the assessment of the serotonergic mechanisms role in the hemodynamics regulation. The special attention is given to the role of various serotonin receptors involved in the gastrointestinal tract motility regulation, in particular located in the digestive system vessel walls. It is known that serotonin has a dual effect on the vessel lumen, due to the heterogeneity of serotonin receptors, which are part of the vascular wall, and different sensitivity of serotonin receptors. Mechanisms at various levels, from central to local, are able to participate in the serotonergic regulation of the vascular lumen, as well as in motility control. According to our data, in the regulation of the upper gastrointestinal tract motor activity participate 5-HT1B- and 5-HT3-receptors located in the stomach and intestines autonomic ganglia, 5-HT2B-receptors localized on stomach plexus neurons and on small and large intestine smooth muscles; 5-HT4-receptors located on stomach wall smooth muscles and intraorgan intestinal plexus neurons. According to the literature, vascular wall 5-HT2B- and 5-HT7-receptors provide vasodilation, whereas the 5-HT1B/1D-, 5-HT2A- and 5-HT2B-receptors - vasoconstriction. Significance of plasma free serotonin level for hemodynamic, serotonergic mechanisms for the different types vessels diameter changing, the interaction of serotonin receptors with sympathetic nervous system and their possible role in the vascular tone regulation are described, particularly the role of presynaptic 5-HT1B/1D-receptors, which prevent the catecholamines release by vegetative nerves endings, is established. Different points of view on the serotoninergic regulation issue, existing contradictions, as well as areas for further fundamental and practical research are presented.


2008 ◽  
Vol 7 (4) ◽  
pp. 31-37
Author(s):  
M. A. Medvedev ◽  
M. B. Baskakov ◽  
S. V. Gusakova ◽  
I. V. Kovalyov ◽  
O. S. Melnik ◽  
...  

The influence of modulation of cytoskeleton by colchicine, vinblastine, cytochalasine B and docetaxel on contractile reactions of smooth muscle cells caused by electric stimulus, depolarization, phenylephrine has been investigated by the mechanographical method, by the methods of the double sucrose gup junction. It is established, that induced by a isoosmotic hyperpotassium solution of reduction of smooth muscle of the rat’s aorta, and also caused depolarization stimulus potentials of action and reductions smooth muscle cells from guinea pig urethra, depend more on the condition of microfilaments cytoskeleton than on microtubules. The reduction of smooth muscles cells of an aorta of the rat, caused by isoosmotic striction, is suppressed under the destruction microfilaments whereas the reduction in a hyperosmotic solution depends on a condition of both microfilaments, and microtubules. Cytoskeleton’s microfilaments of aorta’s smooth muscles and microtubules of smooth muscles of cells ureter are involved in mechanisms of action phenylephrine’s action on contractile activity of smooth muscle cells of an aorta and ureter.


Urology ◽  
2013 ◽  
Vol 81 (3) ◽  
pp. 696.e13-696.e18 ◽  
Author(s):  
Alla E. Lychkova ◽  
Luigi Michele Pavone

1984 ◽  
Vol 62 (3) ◽  
pp. 253-258 ◽  
Author(s):  
Matti Vornanen

The role of sarcolemma and especially sodium pump activity in the control of phasic contractile activity of Ca2+ tolerant myocytes was studied using ouabain and rubidium as sodium pump inhibitors. Initially, ouabain increased both the amplitude of shortening and the frequency of phasic contractions. Later, the amplitude began to decline whereas the frequency of beating continued to rise, often terminating in a steady contracture of the myocyte. Rubidium caused a rapid rise of beating frequency, which reached its full effect within 1–5 min and remained steady after that. The stimulation of contraction frequency and the inhibition of Na+–K+ ATPase were correlated in the case of ouabain but not in the case of rubidium. The results suggest that the stimulation of phasic contractions may be caused by increased uptake of cellular calcium through Na+–Ca+ exchange as a consequence of sodium pump inhibition and (or) depolarization of the sarcolemma by ouabain and rubidium.


2020 ◽  
Vol 26 (5) ◽  
pp. 573-580
Author(s):  
L. V. Smaglii ◽  
V. S. Gusakova ◽  
A. M. Gorianova ◽  
E. A. Golovanov ◽  
E. E. Chibisov ◽  
...  

2008 ◽  
Vol 101 (11) ◽  
pp. 1645-1652 ◽  
Author(s):  
Kenneth J. Broadley ◽  
M. Akhtar Anwar ◽  
Amy A. Herbert ◽  
Martina Fehler ◽  
Elen M. Jones ◽  
...  

Trace amines, including tyramine and β-phenylethylamine (β-PEA), are constituents of many foods including chocolate, cheeses and wines and are generated by so-called ‘friendly’ bacteria such as Lactobacillus, Lactococcus and Enterococcus species, which are found in probiotics. We therefore examined whether these dietary amines could exert pharmacological effects on the gut and its vasculature. In the present study we examined the effects of tyramine and β-PEA on the contractile activity of guinea-pig and rat ileum and upon the isolated mesenteric vasculature and other blood vessels. Traditionally, these amines are regarded as sympathomimetic amines, exerting effects through the release of noradrenaline from sympathetic nerve endings, which should relax the gut. A secondary aim was therefore to confirm this mechanism of action. However, contractile effects were observed in the gut and these were independent of noradrenaline, acetylcholine, histamine and serotonin receptors. They were therefore probably due to the recently described trace amine-associated receptors. These amines relaxed the mesenteric vasculature. In contrast, the aorta and coronary arteries were constricted, a response that was also independent of a sympathomimetic action. From these results, we propose that after ingestion, trace amines could stimulate the gut and improve intestinal blood flow. Restriction of blood flow elsewhere diverts blood to the gut to aid digestion. Thus, trace amines in the diet may promote the digestive process through stimulation of the gut and improved gastrointestinal circulation.


2020 ◽  
Vol 36 (2) ◽  
pp. 135-141
Author(s):  
Marek Krzystanek ◽  
Artur Pałasz

Fluoxetine serves as a primary drug for the pharmacological treatment of binge eating. Its activity usually consists in blocking 2C serotonin receptors. This may be considered to be controversial since agonists of this receptor are effective in pharmacological treatment of bulimia. Bulimia episodes occur as a result of a decrease in serotonergic activity in the central nervous system. The mechanism is clinically confirmed. Drugs which increase the activity of the serotonin system in suppressing binge eating proved effective. The anorexigenic effect of drugs which increase the activity of the serotonin system results from the stimulation of serotonin receptors and not from their blocking. Appetite regulation and binge eating are associated with the activity of the dopaminergic and serotonergic systems. Experimental studies conducted so far prove that the increase in dopaminergic activity in the structures of the reward system is caused by stimulation, and not blocking, of serotonin 2C receptors. The anorexigenic effect of proserotonin drugs may also result from the stimulation of type 3 serotonin receptors and possibly 2C on neurons located in the nucleus of solitary tract. The psychopharmacological investigation conducted in this paper revealed the role of 5-HT2C receptors in the pathogenesis of bulimia nervosa and the mechanism of action of fluoxetine in the treatment of binge eating. Based on existing knowledge, the fact that fluoxetine blocks these receptors does not appear to play a significant role in appetite suppression. Due to few experimental works, the problem requires further research.


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