scholarly journals THE CHANGES OF HUMORAL ADRENERGIC REGULATION OF HEART IN ALCOHOL-TREATED RATS

2017 ◽  
Vol 13 (1-2) ◽  
pp. 3-11
Author(s):  
T.I. Panova ◽  
M.I. Koshelnyk ◽  
S.N. Scherbak
Keyword(s):  
Heart Rate ◽  
Adrenergic Receptors ◽  
Sympathoadrenal System ◽  
Basal Secretion ◽  
Adrenergic Regulation ◽  
Adrenergic Drugs ◽  
Genes Expression ◽  
Systemic Manifestations ◽  
Selective Blocker

Relevance. Under the chronic influence of ethanol the genes expression is changed which contain the information about synthesis of adrenergic receptors, epinephrine enzymes. However studies of the systemic manifestations of these changes are unknown. The distortion of the adrenergic drugs effect in an alcohol-treated organism is probable. Objective: to investigate the adrenergic regulation of the heart in alcohol-treated rates by means of variation of the number of β1 receptors and their ligands. Materials and methods. In control (n=10) and alcohol-treated rats chronically for 120 days (n=10) the number of β1-adrenergic receptors (by means of administration of concor cor selective blocker – 0,28 mg/kg) and the quantity of epinephrine in the blood (by means of activation of sympathoadrenal system after sodium caffeine-benzoate injection – 7,14 mg/kg) were varied. The concor cor and caffeine were administered separately and together. The heart rate (HR) was recorded with the help of sphygmomanometer. The results were processed by using MedStat package. Results. In alcohol-treated rats chronically the HR is 27,6±2,5% higher than in the control ones (383,8±12,9 min-1 and 300,8±8,7 min-1). The caffeine administration leads to an increase in heart rate by 11,5±1,1 % in control rats (up to 335,4±9,5 min-1) while it doesn’t affect this index in alcohol-treated rats (389,6±12,6 min-1). The blockade of β1 receptors leads to a decrease in the HR by 7,5±0,7 % (up to 278,2±7,9 min-1) in control rats and by 15,5±1,1 % (up to 324,4±9,3 min-1) in alcohol-treated rats. When co-administration the β1 receptors blocker and caffeine have nivelated the opposite effects of each other in the control rats and HR remained the same (307,0±8,2 min-1); this has resulted in a decrease in the HR by 4,8±1,0 % (up to 365,4±10,9 min-1) in alcohol-treated animals. Conclusions. It is assumed that the basal secretion of epinephrine is increased and the number of β1 receptors is decreased in alcohol-treated rats compared to control ones.

Effects of adrenergic drugs on the coronary circulation of Atlantic salmon (Salmo salar)

1986 ◽  
Vol 64 (2) ◽  
pp. 481-484 ◽  
Author(s):  
A. P. Farrell ◽  
M. S. Graham
Keyword(s):  
Heart Rate ◽  
Coronary Artery ◽  
Atlantic Salmon ◽  
Salmo Salar ◽  
Coronary Circulation ◽  
Adrenergic Stimulation ◽  
Adrenergic Regulation ◽  
Atlantic Salmon Salmo Salar ◽  
Adrenergic Drugs ◽  
Rate Effects

Spontaneously beating hearts from Atlantic salmon (Salmo salar) were used to examine the adrenergic regulation of the perfused coronary circulation. Excitatory α-adrenoceptors (vasoconstriction) dominated over inhibitory β-adrenoceptors (vasodilatation). Increased heart rate via β-adrenergic stimulation was possible with drug injections into the coronary artery. The heart rate effects followed the vasoactive effect by approximately 2 min.

Effect of exercise duration on density and coupling of beta-adrenergic receptors on human mononuclear cells

1989 ◽  
Vol 66 (3) ◽  
pp. 1494-1500 ◽  
Author(s):  
M. J. Frey ◽  
D. Mancini ◽  
D. Fischberg ◽  
J. R. Wilson ◽  
P. B. Molinoff
Keyword(s):  
Heart Rate ◽  
Adrenergic Receptors ◽  
Regulatory Protein ◽  
Nucleotide Binding ◽  
Plasma Norepinephrine ◽  
Base Line ◽  
Guanine Nucleotide ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Guanine Nucleotide Binding

The effect of maximal exercise on lymphocyte beta-adrenergic receptors was examined in 26 normal subjects. Exercise increased O2 consumption (Vo2) from 5 +/- 1 to 50 +/- 4 ml.min-1.kg-1, plasma norepinephrine level from 188 +/- 28 to 2,682 +/- 160 pg/ml, and plasma epinephrine level from 94 +/- 72 to 857 +/- 180 pg/ml. The density of beta-adrenergic receptors on lymphocytes obtained at rest was 31 +/- 3.7 fmol/mg protein; exercise increased the density of receptors by 86 +/- 33% (range 0–257%) to 58.3 +/- 1.5 fmol/mg protein but did not alter the affinity of the receptor for [125I]iodopindolol or the coupling of the receptor to the guanine nucleotide-binding regulatory protein. The density of beta-adrenergic receptors increased progressively throughout exercise and paralleled the increase in heart rate. The magnitude of the change in the density of beta-adrenergic receptors did not correlate with the magnitude of the increase in heart rate, Vo2, or plasma levels of catecholamines. The density of receptors was still elevated 15 min after completion of exercise but fell below base line 1 h after peak exercise to 18.2 +/- 6.7 fmol/mg protein (P less than 0.05 vs. base-line levels). These results demonstrate that exhaustive exercise results in a progressive increase in the number of beta-adrenergic receptors on lymphocyte membranes, followed by a reduction in the density of receptors during the recovery phase of exercise. Despite a significant increase in the level of plasma catecholamines, the receptor remains coupled to the guanine nucleotide-binding regulatory protein.

Beta-adrenergic receptors predict heart rate reactivity to a psychosocial stressor.

1990 ◽  
Vol 52 (6) ◽  
pp. 621-623 ◽  
Author(s):  
P J Mills ◽  
J E Dimsdale ◽  
M G Ziegler ◽  
C C Berry ◽  
R D Bain
Keyword(s):  
Heart Rate ◽  
Adrenergic Receptors ◽  
Beta Adrenergic Receptors ◽  
Psychosocial Stressor ◽  
Heart Rate Reactivity ◽  
Beta Adrenergic

scholarly journals β3 Adrenergic Receptors in the Sinoatrial Node for Heart Rate Regulation

2021 ◽  
Vol 16 ◽  
Author(s):  
Shu Nakao ◽  
Kazuki Yanagisawa ◽  
Tomoe Ueyama ◽  
Koji Hasegawa ◽  
Teruhisa Kawamura
Keyword(s):  
Heart Rate ◽  
Adrenergic Receptors ◽  
Sinoatrial Node ◽  
Rate Regulation ◽  
Heart Rate Regulation

Cardiovascular effects of dobutamine during exercise in dogs

1989 ◽  
Vol 257 (3) ◽  
pp. H954-H960
Author(s):  
G. C. Haidet ◽  
T. I. Musch ◽  
D. B. Friedman ◽  
G. A. Ordway
Keyword(s):  
Skeletal Muscle ◽  
Heart Rate ◽  
Blood Flow ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Maximal Exercise ◽  
Cardiovascular Effects ◽  
Receptor Reserve ◽  
Concomitant Reduction ◽  
Stimulation Of

To test the hypothesis that stimulation of adrenergic receptors in the heart is maximal during maximal exercise, and to determine whether generalized stimulation of adrenergic receptors during strenuous exercise produces significant alterations in the normal regional distribution of blood flow that occurs during exercise, we evaluated the cardiovascular effects of the infusion of dobutamine (40 micrograms.kg-1.min-1) in mongrel dogs during treadmill running. During maximal exercise, the dobutamine infusion resulted in a significant (P less than 0.05) increase in heart rate. Exercise capacity, total body O2 consumption (VO2), and maximal arteriovenous O2 difference, however, each were reduced during the infusion of this drug. A concomitant reduction in maximal blood flow to locomotive skeletal muscle occurred. The infusion of dobutamine also resulted in an increase in heart rate at a strenuous level of submaximal exercise. However, unlike during maximal exercise, VO2 was unchanged. Blood flow to locomotive skeletal muscle increased, and there was a concomitant reduction in arteriovenous O2 difference. Blood flow reductions that normally occur in splanchnic circulations during strenuous and during maximal exercise were generally somewhat attenuated during the infusion of this drug. Thus, dobutamine, a sympathomimetic agent, produces significant cardiovascular effects when infused in high doses during exercise. Our results demonstrate that beta-adrenergic receptor reserve exists in the heart during maximal exercise in dogs. In addition, the peripheral responses that occur during the infusion of the drug provide additional evidence that different degrees of adrenergic receptor reserve normally appear to be present within different regional circulations during strenuous and during maximal exercise.

scholarly journals Adrenergic Regulation of Macrophage-Mediated Innate/Inflammatory Responses in Obesity and Exercise in this Condition: Role of β2 Adrenergic Receptors

2019 ◽  
Vol 19 (8) ◽  
pp. 1089-1099 ◽  
Author(s):  
Eduardo Ortega ◽  
Isabel Gálvez ◽  
Leticia Martín-Cordero
Keyword(s):  
Stress Responses ◽  
Adrenergic Receptors ◽  
Inflammatory Responses ◽  
Low Grade ◽  
Adrenergic Stimulation ◽  
Adrenergic Regulation ◽  
Induce Insulin Resistance ◽  
Antiinflammatory Effects ◽  
Β Adrenergic Receptors

Background: The effects of exercise on the innate/inflammatory immune responses are crucially mediated by catecholamines and adrenoreceptors; and mediations in both stimulatory and anti-inflammatory responses have been attributed to them. Obesity and metabolic syndrome are included among low-grade chronic inflammatory pathologies; particularly because patients have a dysregulation of the inflammatory and stress responses, which can lead to high levels of inflammatory cytokines that induce insulin resistance, contributing to the onset or exacerbation of type 2 diabetes. Macrophages play a crucial role in this obesity-induced inflammation. Although most of the antiinflammatory effects of catecholamines are mediated by β adrenergic receptors (particularly β2), it is not known whether in altered homeostatic conditions, such as obesity and during exercise, innate/ inflammatory responses of macrophages to β2 adrenergic stimulation are similar to those in cells of healthy organisms at baseline. Objective: This review aims to emphasize that there could be possible different responses to β2 adrenergic stimulation in obesity, and exercise in this condition. Methods: A revision of the literature based on the hypothesis that obesity affects β2 adrenergic regulation of macrophage-mediated innate/inflammatory responses, as well as the effect of exercise in this context. Conclusion: The inflammatory responses mediated by β2 adrenoreceptors are different in obese individuals with altered inflammatory states at baseline compared to healthy individuals, and exercise can also interfere with these responses. Nevertheless, it is clearly necessary to develop more studies that contribute to widening the knowledge of the neuroimmune regulation process in obesity, particularly in this context.

Heart rate changes mediate the embryotoxic effect of antiarrhythmic drugs in the chick embryo

2013 ◽  
Vol 304 (6) ◽  
pp. H895-H902 ◽  
Author(s):  
Radka Kockova ◽  
Jarmila Svatunkova ◽  
Jiri Novotny ◽  
Lucie Hejnova ◽  
Bohuslav Ostadal ◽  
...  
Keyword(s):  
Adverse Effect ◽  
Heart Rate ◽  
Cardiac Output ◽  
Adrenergic Receptors ◽  
Developmental Toxicity ◽  
Premature Death ◽  
Chick Embryos ◽  
In Ovo ◽  
Drug Induced ◽  
Β Adrenergic Receptors

A significant increase in cardiovascular medication use during pregnancy occurred in recent years. Only limited evidence on safety profiles is available, and little is known about the mechanisms of adverse effect on the fetus. We hypothesized that drug-induced bradycardia is the leading mechanism of developmental toxicity. Embryotoxicity was tested in ovo after administration of various doses of metoprolol, carvedilol, or ivabradine. Embryonic day (ED) 4 and 8 chick embryos were studied by video microscopy and ultrasound biomicroscopy ex ovo after intraamniotic injection of the drug for a period of 30 min. Stroke volume was calculated by the Simpson method and prolate ellipsoid formula. Significant dose-dependent mortality was achieved in embryos injected with carvedilol and ivabradine. In ED4 embryos, metoprolol, carvedilol, and ivabradine reduced the heart rate by 33%, 27%, and 55%, respectively, compared with controls (6%). In ED8 embryos this effect was more pronounced with a heart rate reduction by 71%, 54%, and 53%, respectively (controls, 36%). Cardiac output decreased in all tested groups but only proved significant in the metoprolol group in ED8 embryos. The number of β-adrenergic receptors showed a downward tendency during embryonic development. A negative chronotropic effect of metoprolol, carvedilol, and ivabradine was increasingly pronounced with embryonic maturity despite a downward trend in the number of β-adrenergic receptors. This effect was associated with reduced cardiac output in chick embryos, probably leading to premature death. Although standard doses of these drugs appear relatively safe, high doses have a potentially adverse effect on the fetus through reduced heart rate.

Regulation of atrial autonomic receptors in experimental cyanotic heart disease

1991 ◽  
Vol 261 (4) ◽  
pp. H1135-H1140 ◽  
Author(s):  
R. Doshi ◽  
E. Strandness ◽  
D. Bernstein
Keyword(s):  
Heart Rate ◽  
Adrenergic Receptors ◽  
Receptor Subtypes ◽  
Receptor Density ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Beta 2 ◽  
The Right ◽  
Chronic Hypoxemia ◽  
Inotropic Responses

During chronic hypoxemia, left ventricular beta-adrenergic receptor density is decreased and a dissociation occurs between increased chronotropic and decreased inotropic responses to chronically elevated sympathetic tone. To determine whether this dissociation was related to alterations in autonomic receptor populations in the right atrium, we studied right atrial cholinergic and beta-adrenergic receptors in chronically hypoxemic newborn lambs and in normoxemic controls. Heart rate response was determined by infusing isoproterenol at 0.1 or 0.5 microgram.kg-1.min-1. Muscarinic receptors were quantified with [3H]quinuclidinyl benzilate and beta-adrenergic receptors with [125I]iodocyanopindolol. Competition with ICI 118,551 was used to determine beta 1- vs. beta 2-receptor subtypes. In the hypoxemic lambs, isoproterenol resulted in a lesser percentage increase in heart rate (hypoxemic, 46 +/- 6% vs. control, 89 +/- 17%, P less than 0.05); however, because baseline heart rate was higher in the hypoxemic lambs (213 +/- 7 vs. 177 +/- 12 beats/min, P less than 0.05), maximal heart rate responses were similar (310 +/- 7 vs. 326 +/- 6 beats/min, NS). There was no change in receptor density or affinity of either muscarinic or beta-adrenergic receptors and no change in the proportion of beta 1- vs. beta 2-receptor subtypes. Thus the dissociation between the chronotropic and inotropic responses to chronic hypoxemia may be in part secondary to a differential regulation of beta-adrenergic receptors between the left ventricle and the right atrium.

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