BETA-ADRENERGIC BLOCKADE OF THE SYMPATHETIC NERVOUS SYSTEM DECELERATES PERIPORTAL FIBROSIS IN ABCB4 KNOCKOUT MICE

2008 ◽  
Vol 46 (01) ◽  
Author(s):  
I Strack ◽  
M Scheffler ◽  
E Konze ◽  
K Wendland ◽  
H Varnholt ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Knockout Mice ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Periportal Fibrosis ◽  
Sympathetic Nervous

Sympathectomy and beta-adrenergic blockade during lung maturation stimulated by TRH and cortisol in fetal sheep

1993 ◽  
Vol 75 (1) ◽  
pp. 141-147 ◽  
Author(s):  
J. C. Schellenberg ◽  
G. C. Liggins ◽  
J. A. Kitterman ◽  
C. C. Lee
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Adrenergic Blockade ◽  
Lung Maturation ◽  
Fetal Sheep ◽  
Beta Adrenergic ◽  
Adrenergic Mechanisms ◽  
Adrenergic Blocker ◽  
Sympathetic Nervous ◽  
6 Hydroxydopamine

To test whether beta-adrenergic mechanisms and the sympathetic nervous system are involved in the synergistic action of thyrotropin-releasing hormone (TRH) and cortisol on lung maturation, fetal sheep (n = 32) were infused from 121 to 128 days of gestation with saline, TRH + cortisol, TRH + cortisol + beta-adrenergic blocker, or TRH + cortisol after chemical sympathectomy with 6-hydroxydopamine. TRH + cortisol increased lung distensibility and stability and alveolar concentrations of saturated phosphatidylcholine two- to threefold over control fetuses. beta-Adrenergic blockade prevented the increase in distensibility in response to TRH + cortisol. Sympathectomy did not impair the increase in distensibility and stability in response to TRH + cortisol but inhibited the increase in alveolar total phospholipids. Tissue concentrations of saturated phosphatidylcholine increased in TRH + cortisol-treated fetuses after either sympathectomy or beta-adrenergic blockade. We concluded that during lung maturation by TRH + cortisol 1) sympathetic mechanisms are requisite for surfactant release, 2) nonneurogenic beta-adrenergic mechanisms are requisite for the maturation of the mechanical properties of the lung and 3) stimulation of surfactant synthesis is independent of beta-adrenergic action and the sympathetic nervous system.

Abnormal Regulation of the Sympathetic Nervous System in α2A-Adrenergic Receptor Knockout Mice

1999 ◽  
Vol 56 (1) ◽  
pp. 154-161 ◽  
Author(s):  
John D. Altman ◽  
Anne U. Trendelenburg ◽  
Leigh MacMillan ◽  
Dan Bernstein ◽  
Lee Limbird ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Knockout Mice ◽  
Adrenergic Receptor ◽  
Sympathetic Nervous

Ontogeny of canine intrathoracic cardiac nervous system

1991 ◽  
Vol 261 (4) ◽  
pp. R920-R927 ◽  
Author(s):  
C. Haddad ◽  
J. A. Armour
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Adrenergic Receptors ◽  
Beta Agonist ◽  
Canine Heart ◽  
Cardiac Innervation ◽  
Beta Adrenergic Receptors ◽  
Parasympathetic Innervation ◽  
Beta Adrenergic ◽  
Sympathetic Nervous

The functional cardiac innervation of 61 puppies from nine different litters (2-8 littermates), ranging in age from 1 day to 7 wk, was investigated. The efferent sympathetic nervous system exerted minimal effects on the heart of 1-day-old puppies, gradually influencing the heart more thereafter such that by 7 wk of life it was functionally mature. In contrast, efferent parasympathetic cardiac innervation was well developed at birth, maturing thereafter such that by 4-7 wk of age its capacity to modulate the heart was similar to that found in adults. The right- and left-sided efferent sympathetic and parasympathetic intrathoracic nervous systems induced similar cardiac modulation throughout this period of development. Cardiac myocyte beta-adrenergic receptors were partially functional at birth, as determined by responses elicited by supramaximal doses of the beta-agonist isoproterenol. Responses elicited by isoproterenol became greater over the following 7 wk of life, when they were found to be similar to those elicited in adults. By 1 wk of age, synaptic mechanisms in intrathoracic sympathetic ganglia involved in cardiac regulation were relatively well developed, with cardiopulmonary-cardiac reflexes present but not functionally mature at that age. It is concluded that maturation of the efferent sympathetic nervous system modulating the canine heart depends to a large extent on the ontogeny of cardiac beta-adrenergic receptors rather than the ontogeny of synapses in intrathoracic ganglia. Furthermore, even though functional cardiac efferent parasympathetic innervation is present before efferent sympathetic innervation, both reach maturity at about the same age.

BETA-ADRENERGIC MEDIATION OF SYMPATHETIC NERVOUS SYSTEM ACTIVITY

1982 ◽  
Vol 10 (3) ◽  
pp. 221
Author(s):  
Bart Chernow ◽  
Michael Ziegler ◽  
Joseph Coyle ◽  
David Cruess ◽  
Pat Hughes ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nervous System Activity ◽  
Beta Adrenergic ◽  
System Activity ◽  
Nervous System Activity ◽  
Sympathetic Nervous

Abnormal cardiac function associated with sympathetic nervous system hyperactivity in mice

2002 ◽  
Vol 283 (5) ◽  
pp. H1838-H1845 ◽  
Author(s):  
Patricia C. Brum ◽  
Jon Kosek ◽  
Andrew Patterson ◽  
Daniel Bernstein ◽  
Brian Kobilka
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Cardiac Function ◽  
Knockout Mice ◽  
Cardiac Tissue ◽  
Cardiac Contractility ◽  
Peak Oxygen Uptake ◽  
Sympathetic Tone ◽  
Relevant Animal Model ◽  
Sympathetic Nervous

α2A-Adrenergic receptors (ARs) in the midbrain regulate sympathetic nervous system activity, and both α2A-ARs and α2C-ARs regulate catecholamine release from sympathetic nerve terminals in cardiac tissue. Disruption of both α2A- and α2C-ARs in mice leads to chronically elevated sympathetic tone and decreased cardiac function by 4 mo of age. These knockout mice have increased mortality, reduced exercise capacity, decreased peak oxygen uptake, and decreased cardiac contractility relative to wild-type controls. Moreover, we observed significant abnormalities in the ultrastructure of cardiac myocytes from α2A/α2C-AR knockout mice by electron microscopy. Our results demonstrate that chronic elevation of sympathetic tone can lead to abnormal cardiac function in the absence of prior myocardial injury or genetically induced alterations in myocardial structural or functional proteins. These mice provide a physiologically relevant animal model for investigating the role of the sympathetic nervous system in the development and progression of heart failure.

scholarly journals Indirect autonomic nervous system activity assessment in patients with myocardial infarction

2021 ◽  
Vol 10 (Supplement_1) ◽  
Author(s):  
VA Aleksandrenko ◽  
EA Kuzheleva ◽  
AA Garganeeva
Keyword(s):  
Myocardial Infarction ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Sympathetic Nervous System ◽  
Autonomic Nervous System Activity ◽  
Beta Adrenergic ◽  
System Activity ◽  
Autonomic Nervous ◽  
Nervous System Activity ◽  
Sympathetic Nervous

Abstract Funding Acknowledgements Type of funding sources: None. Introduction. Abnormalities in the cardiac sympathetic nervous system have been documented in myocardial infarction (MI) and have been directly implicated in pathogenesis and progression of MI. Assessment of the autonomic nervous system activity in acute stage of MI allowed us to identify groups of high-risk patients. Purpose. To investigate the sympathetic nervous system activity in patients with MI by assessing the condition of beta-adrenergic reactivity of erythrocytes. To analyze ADRB1 Arg389Gly associations with the state of beta-adrenergic reactivity of erythrocytes in patients with MI. Methods. During the study period, 62 patients were enrolled. The patients were divided into 2 groups. The first group consisted of 11 patients (nine women and two men, median age of 54.0 [49.0;61.0] years) with normal beta-adrenergic reactivity of erythrocytes, the second group consisted of 51 patients (40 women and 11 man, median age of 61.0 [48.0;72.0] years) with abnormal beta-adrenergic reactivity of  erythrocytes. The research of beta-adrenergic reactivity of erythrocytes was conducted by analysis of changing erythrocyte osmoresistance under the influence of beta blocker in the first 6 hours from the onset of the heart attack. The genetic research was conducted by PСR method in real time. Results. Groups of patients were comparable in main clinical indicators (anamnesis of ischemic heart disease and chronic heart failure, frequency of beta blockers administration before and during of MI, electrocardiography features: elevation of ST-segment, Q-wave and etc.). The second group presented with a higher occurrence of acute left ventricular failure (33.3% vs 0%, p = 0.026) and arterial hypertension (90.2% vs 63.6%, p = 0.044). Parameters of myocardial damage were significantly higher in the second group than the first group. Primarily, this manifested in the presence of a greater number of hypokinesis zones on echocardiography (p = 0.015). In addition, patients of the second group had a lower ejection fraction according to echocardiography (51.0 [46.5;59.0]% vs 58.0 [52.0;63.0]%, p = 0.042). Levels of blood necrosis biomarkers were significantly higher in the second group, e.g. Troponin I (24.1 [9.9;68.0] ng/ml vs 1.3 [0.2;1.8] ng/ml, p = 0.001). At the same time statistically significant distinctions of the severity of coronary atherosclerosis in groups were not revealed. The analysis of ADRB1 Arg389Gly demonstrated association of CC-genotype with abnormal beta-adrenergic reactivity of erythrocytes [OR 5.9, 95% СI 1.16-30.25, p = 0.043]. Conclusion. Patients with an abnormal beta-adrenergic reactivity were characterized by a greater volume of damage to the heart muscle. Moreover, association of CC-genotype of gene ADRB1 Arg389Gly with abnormal beta-adrenergic reactivity of erythrocytes was identified.

scholarly journals Contribution of Sympathetic Nervous System to High Blood Pressure in Salt Hypertensive Dahl Rats

2021 ◽  
pp. 117-118
Author(s):  
Josef Zicha
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Salt Intake ◽  
Adrenergic Blockade ◽  
Control Groups ◽  
Adrenergic Mechanisms ◽  
Salt Hypertension ◽  
Sympathetic Nervous

The important participation of sympathetic nervous system in various forms of experimental hypertension is well known. This is also true for salt hypertension elicited by excess salt intake in Dahl salt-sensitive rats (for review see Zicha et al. 2012). Two recent studies in Dahl rats (Zicha et al. 2019, Puleo et al. 2020) evaluated the hypothesis on the role of β-adrenergic WNK4-NCC pathway in salt-sensitive hypertension which has been proposed by Mu et al. (2011). Although these studies differed in many experimental details, both of them demonstrated a major importance of α1- rather than β adrenergic mechanisms for the development of salt hypertension in this rat strain. Zicha et al. (2019) demonstrated that chronic β adrenergic blockade by propranolol did not lower blood pressure (BP) in Dahl salt-sensitive rats developing salt hypertension. It also did not modify their sympathetic component or natriuretic response to acute hydrochlorothiazide administration which inhibited the activity of sodium-chloride cotransporter (NCC). Puleo et al. (2020) reported that chronic β-adrenergic blockade failed to affect salt hypertension development or to reduce renal WNK4-NCC pathway. On the other hand, their study demonstrated the important influence of α1 adrenergic pathway on the activity, expression and phosphorylation of NCC. Chronic α1-adrenergic antagonism by terazosin treatment in Dahl salt-sensitive rats, which started before the onset of high salt intake, considerably attenuated the development of salt hypertension. This treatment diminished BP difference between the salt-loaded Dahl salt-sensitive rats and their control groups by 70-75 %. However, terazosin-treated Dahl salt-sensitive animals fed a high-salt diet had not only suppressed renal NCC activity but they also did not respond to acute phenylephrine administration. This suggests that chronic α1-adrenergic blockade affected both renal sodium retention mechanisms and α1-adrenergic vasoconstriction (Puleo et al. 2020). It remains to determine how these two mechanisms contribute to salt hypertension in Dahl rats. We found that the acute ganglionic blockade lowered substantially BP of salt hypertensive Dahl rats, abolishing 45-55 % of the BP difference between salt-loaded Dahl salt-sensitive rats and their control groups (Zicha et al. 2019). If we consider the results of both above studies, it seems that the renal contribution might be responsible for about 25 % of BP elevation seen in Dahl salt-sensitive rats developing salt hypertension, whereas α1-adrenergic vasoconstriction contributes to this BP change by about 50 %. Of course, this consideration is highly speculative. Nevertheless, it might stimulate further effort to distinguish the role of kidney and brain in the pathogenesis of salt hypertension. Perhaps even more promising could be the estimation of renal and extrarenal effects of central sympathoexcitation in Dahl rats (Mark 1991, Gabor and Leenen 2012, Fujita et al. 2009) which is related to central α2-adrenergic mechanisms (Wainford et al. 2015). As far as the role of kidney in the pathogenesis of salt hypertension is concerned (Frame et al. 2019), some attention should also be paid to participation of renal vascular and tubular effects of increased sympathetic tone in these salt hypertensive animals.

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