scholarly journals Beta-Adrenoceptor Modulation in a Case of Pure Autonomic Failure

1992 ◽  
Vol 19 (1) ◽  
pp. 80-83
Author(s):  
Sergio Perna ◽  
Rocco Leone ◽  
Maria Jussie Farace ◽  
Vincenzo Brescia-Morra ◽  
Giuseppe Campanella ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Autonomic Dysfunction ◽  
Autonomic Failure ◽  
Plasma Catecholamines ◽  
Pure Autonomic Failure ◽  
Beta Adrenoceptor ◽  
The Poor ◽  
Sympathetic Nervous ◽  
Isoproterenol Infusion

ABSTRACT:In a patient with pure autonomic failure, exercise did not modify beta-adrenoceptor density, probably due to an insufficient increase in plasma catecholamines. Isoproterenol infusion increased the number of beta-adrenoceptor by only 17%. Since in control subjects an increased beta-adrenoceptor level was found, following both physical stress and isoproterenol infusion, we suggest that the lack of increased beta-adrenoceptor levels may contribute to the poor circulatory adjustments observed in autonomic dysfunction during activities involving the sympathetic nervous system.

Neurovascular Role of Sympathetic Nervous System and Beta-Adrenoceptor Polymorphisms in Obesity and Hypertension

2008 ◽  
Vol 4 (2) ◽  
pp. 121-130 ◽  
Author(s):  
Kazuko Masuo ◽  
Gavin Lambert ◽  
Hiromi Rakugi ◽  
Toshio Ogihara ◽  
Murray Esler
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Beta Adrenoceptor ◽  
Sympathetic Nervous

Ethnic differences in sympathetic nervous system-mediated energy expenditure

1991 ◽  
Vol 261 (6) ◽  
pp. E789-E794 ◽  
Author(s):  
M. F. Saad ◽  
S. A. Alger ◽  
F. Zurlo ◽  
J. B. Young ◽  
C. Bogardus ◽  
...  
Keyword(s):  
Nervous System ◽  
Energy Expenditure ◽  
Sympathetic Nervous System ◽  
Fat Mass ◽  
Weight Maintenance ◽  
Resting Metabolic Rate ◽  
Fat Free Mass ◽  
Beta Adrenoceptor ◽  
Sympathetic Nervous ◽  
The Impact

The impact of sympathetic nervous system (SNS) activity on energy expenditure (EE) was evaluated in nondiabetic Caucasian and Pima Indian men while on a weight-maintenance diet using two approaches as follows. 1) The relationship between 24-h EE, measured in a respiratory chamber, and 24-h urinary norepinephrine was studied in 36 Caucasians [32 +/- 8 (SD) yr, 95 +/- 41 kg, 22 +/- 13% fat] and 33 Pimas (29 +/- 6 yr, 103 +/- 28 kg, 30 +/- 9% fat). There was no difference between the two groups in 24-h EE (2,422 vs. 2,523 kcal/24 h) and in urinary norepinephrine (28 vs. 31 micrograms/24 h), even after adjusting for body size and composition. Twenty-four-hour EE correlated significantly with 24-h urinary norepinephrine in Caucasians (r = 0.78, P less than 0.001) but not in Pimas (r = 0.03), independent of fat-free mass (FFM), fat mass, and age. 2) The effect of beta-adrenoceptor blockade with propranolol (120 micrograms/kg FFM bolus and 1.2 micrograms.kg FFM-1.min-1 for 45 min) on the resting metabolic rate (RMR) was evaluated in 36 Caucasians (30 +/- 6 yr, 103 +/- 36 kg, 25 +/- 11% fat) and 32 Pimas (28 +/- 6 yr, 100 +/- 34 kg, 27 +/- 10% fat). The RMR was similar in the two groups (2,052 vs. 1,973 kcal/24 h) even after adjustment for FFM, fat mass, and age and dropped significantly after propranolol infusion in Caucasians (-3.9%, P less than 0.001) but not in Pimas (-0.8%, P = 0.07).(ABSTRACT TRUNCATED AT 250 WORDS)

Role of the sympathetic nervous system in the alcohol–guanabenz hemodynamic interaction

1992 ◽  
Vol 70 (9) ◽  
pp. 1217-1224 ◽  
Author(s):  
Abdel A. Abdel-Rahman ◽  
Robert G. Carroll ◽  
Mahmoud M. El-Mas
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Spontaneously Hypertensive Rats ◽  
Specific Interaction ◽  
Plasma Catecholamines ◽  
Hypotensive Effect ◽  
Plasma Catecholamine ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Sympathetic Nervous

The present study evaluated the contribution of the sympathetic nervous system to the adverse hemodynamic action of ethanol on hypotensive responses in conscious unrestrained spontaneously hypertensive rats. Ethanol caused a dose-related attenuation of the hypotensive effect of guanabenz. An equivalent hypotensive response to sodium nitroprusside was not influenced by ethanol, which indicates a potential specific interaction between ethanol and guanabenz. Alternatively, it is possible that a preexisting high sympathetic nervous system activity, which occurred during nitroprusside infusion, may mask a sympathoexcitatory action of ethanol. Further, ethanol (1 g/kg) failed to reverse the hypotensive effect of the ganglionic blocker hexamethonium. This suggests that a centrally mediated sympathoexcitatory action of ethanol is involved, at least partly, in the reversal of hypotension. In addition, the antagonistic interaction between ethanol and guanabenz seems to take place within the central nervous system and involves opposite effects on central sympathetic tone. Finally, changes in plasma catecholamines provide supportive evidence for the involvement of the sympathetic nervous system in this interaction. In a separate group of conscious spontaneously hypertensive rats, ethanol (1 g/kg) reversed the guanabenz-evoked decreases in blood pressure and plasma catecholamine levels. It is concluded that (i) ethanol adversely interacts with centrally acting antihypertensive drugs through a mechanism that involves a directionally opposite effect on sympathetic activity, and (ii) a sympathetically mediated pressor effect of ethanol is enhanced in the presence of an inhibited central sympathetic tone.Key words: spontaneously hypertensive rats, ethanol, catecholamines, guanabenz, hexamethonium.

Pentobarbital effects on plasma catecholamines: temperature, heart rate, and blood pressure

1985 ◽  
Vol 248 (1) ◽  
pp. E95-E100 ◽  
Author(s):  
D. Baum ◽  
J. B. Halter ◽  
G. J. Taborsky ◽  
D. Porte
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Animal Models ◽  
Sympathetic Nervous System ◽  
Rectal Temperature ◽  
Plasma Catecholamines ◽  
Plasma Catecholamine ◽  
Sympathetic Nervous ◽  
Plasma Catecholamine Concentrations

The effects of intravenous pentobarbital were studied in dogs. Plasma pentobarbital concentrations were inversely related to epinephrine and norepinephrine concentrations. Plasma catecholamines appeared fully suppressed at pentobarbital levels greater than 25-30 micrograms/ml. Furthermore, pentobarbital levels were negatively related to rectal temperature, heart rate, and mean blood pressure. The methods of pentobarbital administration influenced plasma pentobarbital as well as epinephrine and norepinephrine levels, temperature, heart rate, and blood pressure. These observations suggest the possibility that pentobarbital inhibits the sympathetic nervous system, which in turn may affect temperature, heart rate, and blood pressure. Because pentobarbital anesthesia affects plasma catecholamine concentrations, the regimen used in animal models requires consideration when interpreting data potentially influenced by the sympathetic nervous system.

Plasma Dopamine β-Hydroxylase and Noradrenaline Amounts in Essential Hypertension

1973 ◽  
Vol 44 (6) ◽  
pp. 617-620 ◽  
Author(s):  
L. B. Geffen ◽  
R. A. Rush ◽  
W. J. Louis ◽  
A. E. Doyle
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Essential Hypertension ◽  
Sympathetic Nervous System ◽  
Diastolic Blood Pressure ◽  
Plasma Catecholamines ◽  
Plasma Noradrenaline ◽  
Elevated Blood Pressure ◽  
Elevated Blood ◽  
Sympathetic Nervous

1. Plasma dopamine β-hydroxylase (DβH) amounts were measured by radioimmunoassay in twenty-eight patients, twenty of whom had essential hypertension. There was a positive correlation between resting diastolic blood pressure and plasma DβH concentration. 2. Plasma DβH amounts also correlated significantly with those of plasma noradrenaline (NA) in individual patients. 3. These findings provide further support for the conclusions drawn from studies of plasma catecholamines that the sympathetic nervous system contributes toward the maintenance of the elevated blood pressure in essential hypertension.

scholarly journals Social instability and immunity in rhesus monkeys: the role of the sympathetic nervous system

2015 ◽  
Vol 370 (1669) ◽  
pp. 20140104 ◽  
Author(s):  
John P. Capitanio ◽  
Steven W. Cole
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Lymph Nodes ◽  
Rhesus Monkeys ◽  
Plasma Catecholamines ◽  
Social Conditions ◽  
Type I ◽  
Social Instability ◽  
Stable Conditions ◽  
Sympathetic Nervous

Social instability can adversely affect endocrine, immune and health outcomes, and recent evidence suggests that the sympathetic nervous system (SNS) might mediate these effects. We conducted two studies with adult male rhesus monkeys ( Macaca mulatta ) to understand how social conditions affect measures of SNS activity and immune function. In Experiment 1, animals were socialized in stable social conditions, then were switched to unstable (stressful) social conditions, then were returned to stable conditions. Analysis revealed quadratic effects for measures of behaviour, urinary metabolites of epinephrine and norepinephrine, and expression of immune response genes: as expected, social instability adversely impacted most measures, and the effects remediated upon re-imposition of stable conditions. Cortisol levels were unaffected. In Experiment 2, we used the sympathomimetic drug methamphetamine to challenge the SNS; animals also underwent socialization in stable or unstable groups. Surprisingly, while methamphetamine elevated plasma catecholamines, responses in lymph nodes tracked the social, and not the drug, condition: social instability upregulated the density of SNS fibres in lymph nodes and downregulated Type I interferon gene expression. Together, these results indicate that the SNS is extremely sensitive to social conditions; full understanding of the adverse effects of social instability on health should therefore incorporate measures of this health-relevant system.

Involvement of sympathetic nervous system and brown fat in endotoxin-induced fever in rats

1988 ◽  
Vol 255 (5) ◽  
pp. E617-E620 ◽  
Author(s):  
M. M. Jepson ◽  
D. J. Millward ◽  
N. J. Rothwell ◽  
M. J. Stock
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Brown Adipose ◽  
Sympathetic Nervous ◽  
Escherichia Coli Lipopolysaccharide ◽  
Marked Suppression

The object of this study was to assess the role of brown adipose tissue (BAT) and the sympathetic nervous system in the rise in heat production associated with endotoxin-induced fever. Oxygen consumption (VO2) was found to be significantly increased (28%) over a 4-h period after two doses of endotoxin (Escherichia coli lipopolysaccharide, 0.3 mg/100 g body wt) given 24 h apart. Injection of a mixed beta-adrenoceptor antagonist (propranolol) reduced VO2 by 14% in endotoxin-treated rats, whereas the selective beta 1- (atenolol) or beta 2- (ICI 118551) antagonists suppressed VO2 by 10%. These drugs did not affect VO2 in control animals. BAT thermogenic activity assessed from measurements of in vitro mitochondrial guanosine 5'-diphosphate (GDP) binding was elevated by 54% in interscapular BAT and by 171% in other BAT depots. Surgical denervation of one lobe of the interscapular depot prevented these responses. Endotoxin failed to stimulate GDP binding in rats fed protein-deficient diets. This may have been because BAT thermogenic activity was already elevated in control rats fed these diets or because endotoxin caused a marked suppression of food intake in the protein-deficient animals. The results indicate that sympathetic activation of BAT is involved in the thermogenic responses to endotoxin and that these can be modified by dietary manipulation.

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