Age-Dependence of Noradrenaline Kinetics in Normal Subjects

1981 ◽  
Vol 60 (2) ◽  
pp. 217-219 ◽  
Author(s):  
M. Esler ◽  
H. Skews ◽  
P. Leonard ◽  
G. Jackman ◽  
A. Bobik ◽  
...  
Keyword(s):  
Nervous System ◽  
Healthy Subjects ◽  
Plasma Clearance ◽  
Normal Subjects ◽  
Plasma Noradrenaline ◽  
Age Dependence ◽  
Plasma Noradrenaline Concentration ◽  
Noradrenaline Concentration ◽  
Sympathetic Nervous ◽  
Older Subjects

1. The influence of age on the rate of spillover of noradrenaline into plasma, clearance of noradrenaline from plasma, and plasma noradrenaline concentration at rest was studied in 34 healthy subjects aged 20–69 years. 2. The plasma concentration of noradrenaline was dependent on age, values being higher in older subjects. 3. This age-dependence of plasma noradrenaline concentration was due principally to a reduced clearance of noradrenaline from the circulation in older subjects. 4. The rate of spillover of noradrenaline into plasma was little influenced by age. The higher plasma noradrenaline values found in older subjects do not seem to be due to an increase in sympathetic nervous system tone with aging.

Reduced plasma noradrenaline concentrations in simple-obese and diabetic obese patients

1991 ◽  
Vol 80 (1) ◽  
pp. 53-58 ◽  
Author(s):  
Arne V. Astrup ◽  
Niels Juel Christensen ◽  
Leif Breum
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Plasma Noradrenaline ◽  
Obese Group ◽  
Diabetic Patients ◽  
Obese Patients ◽  
Plasma Noradrenaline Concentration ◽  
Fasting Plasma ◽  
Noradrenaline Concentration ◽  
Sympathetic Nervous

1. Obesity may be associated with a decreased activity of the sympathetic nervous system and also with a deficiency of the response to stimuli activating the sympathetic nervous system. As insulin activates the sympathetic nervous system, the present study was undertaken to measure the plasma noradrenaline concentration in the fasting state and after 75 g of oral glucose in simple-obese patients (n = 13), in non-insulin-dependent (type 2) diabetic patients (n = 37) and in normal control subjects (n = 12). 2. The fasting plasma noradrenaline concentration was similarly reduced in the simple-obese group and in the diabetic obese group compared with the control group (P = 0.005). The glucose-induced increase in plasma noradrenaline concentration was normal in the simple- obese group, but was abolished in the obese diabetic patients (P = 0.008). 3. Step-wise regression analysis indicated that independent effects on the fasting plasma noradrenaline concentration were exerted by age (r = + 0.32, P = 0.002), glucose concentration (r = −0.32, P = 0.02) and the degree of obesity (r = −0.37, P = 0.007), but not by plasma insulin concentration. 4. These results show that obese patients have a reduced fasting plasma noradrenaline concentration independently of accompanying diabetes, but that the response of noradrenaline to oral glucose is only abolished in the obese diabetic patients.

Determination of Noradrenaline Uptake, Spillover to Plasma and Plasma Concentration in Patients with Essential Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 311s-313s ◽  
Author(s):  
M. Esler ◽  
G. Jackman ◽  
P. Leonard ◽  
A. Bobik ◽  
Helen Skews ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Normal Subjects ◽  
Plasma Noradrenaline ◽  
Neuronal Uptake ◽  
Noradrenaline Uptake ◽  
Plasma Noradrenaline Concentration ◽  
Noradrenaline Concentration ◽  
Uptake Of Noradrenaline ◽  
Rapid Removal ◽  
Autonomic Insufficiency

1. The rates of entry of noradrenaline to plasma and of removal of noradrenaline from plasma, and plasma noradrenaline concentration, were determined in normal subjects and in patients with essential hypertension. Neuronal uptake of noradrenaline was assessed from the plasma tritiated noradrenaline disappearance curve, after infusion to steady state. 2. Noradrenaline disappearance was biexponential. Rapid removal was dependent on neuronal uptake, being slowed if neuronal noradrenaline uptake was reduced, either by desipramine in normal subjects, or in patients with sympathetic nerve dysfunction (autonomic insufficiency). 3. In 10 of 41 hypertensive patients the t1 1/2 similarly was prolonged, presumptive evidence of a defect in neuronal noradrenaline uptake. Endogenous noradrenaline escaping uptake after release, and spilling over into plasma, and plasma noradrenaline concentration, were increased in these patients. 4. Defective neuronal uptake of noradrenaline, by exposing adrenoreceptors to high local transmitter concentration, may be important in the pathogenesis of essential hypertension in some patients.

Plasma and platelet free catecholamine concentrations in patients with familial hypercholesterolaemia

1992 ◽  
Vol 82 (1) ◽  
pp. 113-116 ◽  
Author(s):  
C. C. T. Smith ◽  
B. N. C. Prichard ◽  
D. J. Betteridge
Keyword(s):  
Familial Hypercholesterolaemia ◽  
Plasma Cholesterol ◽  
Normal Subjects ◽  
Plasma Noradrenaline ◽  
Cholesterol Concentration ◽  
Plasma Cholesterol Concentration ◽  
Plasma Noradrenaline Concentration ◽  
Noradrenaline Concentration ◽  
Heterozygous Familial Hypercholesterolaemia ◽  
Noradrenaline Levels

1. Plasma and platelet free catecholamine concentrations were measured in 22 normal subjects and in 10 treated and 11 untreated patients with heterozygous familial hypercholesterolaemia. 2. Plasma noradrenaline concentrations were significantly higher in both treated and untreated hypercholesterolaemic patients than in normal subjects. Adrenaline concentrations did not differ. 3. Platelet noradrenaline levels were higher in untreated hypercholesterolaemic patients than in normal subjects. 4. Positive correlations between the plasma noradrenaline concentration and the platelet noradrenaline concentration were observed in both normal subjects and hypercholesterolaemic patients. 5. Combining the data for normal subjects and hypercholesterolaemic patients revealed that the plasma noradrenaline concentration correlated positively with the plasma cholesterol concentration. The platelet noradrenaline concentration was also found to correlate with the plasma cholesterol concentration. 6. Our results suggest that an increased plasma cholesterol concentration may be associated with increased sympathetic nervous system activity as indicated by elevated plasma and platelet noradrenaline levels. Increases in circulating catecholamines may contribute to the platelet hyperaggregability seen in familial hypercholesterolaemia.

Endogenous Agonist Regulation of α-Adrenoceptors in Man

1981 ◽  
Vol 61 (s7) ◽  
pp. 207s-210s ◽  
Author(s):  
I. B. Davies ◽  
D. Sudera ◽  
P. S. Sever
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Inverse Relationship ◽  
Normal Subjects ◽  
Plasma Noradrenaline ◽  
Adrenergic Agonist ◽  
Receptor Affinity ◽  
System Degeneration ◽  
Receptor Number ◽  
Sympathetic Nervous

1. Plasma noradrenaline concentrations and platelet α-receptor properties were measured in 14 normal subjects, five phaeochromocytoma patients and nine patients with multiple system atrophy and sympathetic nervous system degeneration (MSA). 2. Plasma noradrenaline concentrations in phaeochromocytoma were 10- to 20-times greater than those of normal subjects and one-fifth to one-half of normal in MSA patients. 3. Platelet α-receptor numbers were increased in MSA and decreased in phaeochromocytoma compared with normal subjects. There was no change in platelet α-receptor affinity in either group. 4. The inverse relationship between α-receptor numbers and plasma noradrenaline concentrations may reflect regulation of α-receptor number by endogenous adrenergic agonist concentrations in man.

Variations in Individual Organ Release of Noradrenaline Measured by An Improved Radioenzymatic Technique; Limitations of Peripheral Venous Measurements in the Assessment of Sympathetic Nervous Activity

1981 ◽  
Vol 61 (5) ◽  
pp. 585-590 ◽  
Author(s):  
M. J. Brown ◽  
D. A. Jenner ◽  
D. J. Allison ◽  
C. T. Dollery
Keyword(s):  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Nervous Activity ◽  
Artery Stenosis ◽  
Plasma Noradrenaline ◽  
Sympathetic Nervous Activity ◽  
Release Of Noradrenaline ◽  
Noradrenaline Concentration ◽  
Sympathetic Nervous ◽  
Noradrenaline And Adrenaline

1. The validity of plasma noradrenaline as an index of sympathetic nervous activity was assessed by estimating variation in individual organ contribution to circulating concentrations. 2. Arteriovenous (A—V) differences in noradrenaline and adrenaline concentration were measured across several organs in nine patients with mild essential hypertension, in five with renal artery stenosis and 15 phaeochromocytoma patients. 3. In patients with phaeochromocytomas the percentage extraction of noradrenaline and adrenaline (estimated from the A—V differences) was similar across all organs, suggesting that adrenaline extraction could be used as a marker for noradrenaline extraction. 4. In the non-tumour patients the A—V difference for noradrenaline was less than that for adrenaline across most organs studied, reflecting the net result of noradrenaline release and extraction. The estimated contribution of various organs to the noradrenaline concentrations in their venous effluent was: heart. 21%; kidney 47%; legs 68%. 5. This pattern of A—V difference proved a positive diagnostic feature for non-tumour patients since it was not found even in the patients with small phaeochromocytomas, whose peripheral venous noradrenaline concentration alone did not distinguish them. 6. The venous-arterial difference across the adrenal glands of non-tumour patients was more than 10-fold greater for adrenaline than that for noradrenaline. Since the mean arterial concentration of noradrenaline was more than fivefold higher than that of adrenaline, the normal adrenal contribution to circulating noradrenaline is likely to be less than 2%. 7. In the patients with renal artery stenosis renal venous concentrations of noradrenaline (from the ischaemic kidney) were higher than arterial values, but mean arterial values were no higher than in the essential hypertensive patients. 8. Local variations in sympathetic activity may occur without altering the plasma noradrenaline concentration measured in peripheral plasma.

scholarly journals Increase in plasma noradrenaline concentration after the administration of phentolamine in the patients with "latent" left-sided heart failure.

1989 ◽  
Vol 53 (12) ◽  
pp. 1497-1505 ◽  
Author(s):  
HIROKO WATANABE ◽  
HIROYASU ITO ◽  
SHINYA MINATOGUCHI ◽  
YOKO IMAI ◽  
MASATOSHI KOSHIJI ◽  
...  
Keyword(s):  
Heart Failure ◽  
Plasma Noradrenaline ◽  
Plasma Noradrenaline Concentration ◽  
Noradrenaline Concentration

Influence of the Sympathetic Nervous System on Aortic Compliance

1980 ◽  
Vol 59 (s6) ◽  
pp. 279s-282s ◽  
Author(s):  
C. L. Alicandri ◽  
R. Fariello ◽  
E. Agabiti-Rosei ◽  
G. Romanelli ◽  
G. Muiesan
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Stroke Volume ◽  
Pulse Pressure ◽  
Plasma Noradrenaline ◽  
Aortic Compliance ◽  
Sympathetic Nervous ◽  
Group 2 ◽  
Group 1 ◽  
Noradrenaline Levels

1. Aortic compliance and plasma catecholamine levels were determined in 26 essential hypertensive patients: 14<45 years (group 1) and 12>45 years (group 2). 2. Aortic rigidity, the reciprocal of aortic compliance, was calculated by the ratio of pulse pressure to stroke volume. Pulse pressure was derived by arterial pressure measured in the ascending aorta. Stroke volume was obtained by dye dilution. 3. A significant correlation (r = 0.60) was found between aortic rigidity and plasma noradrenaline in group 2. In this group both aortic rigidity and plasma noradrenaline levels were consistently higher than in group 1. 4. In 15 patients (seven of group 1 and eight of group 2) aortic rigidity was again measured after acute phentolamine (five patients) and labetalol (ten patients) administration. 5. Aortic rigidity was reduced significantly after both α-adrenoreceptor blockade alone and combined α- and β-adrenoreceptor blockade. A highly significant correlation was found between aortic rigidity reduction and pretreatment noradrenaline levels (r = 0.77). 6. Aortic compliance is influenced, at least in part, by sympathetic nervous system activity. Drugs which block the peripheral effects of catecholamines may improve aortic compliance and consequently the control of systolic hypertension in selected cases.

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