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.

Choice of Control Groups in the Appraisal of Sympathetic Nervous Activity in Essential Hypertension

1979 ◽  
Vol 57 (4) ◽  
pp. 339-344 ◽  
Author(s):  
D. H. Jones ◽  
Carlene A. Hamilton ◽  
J. L. Reid
Keyword(s):  
Essential Hypertension ◽  
Nervous Activity ◽  
Plasma Noradrenaline ◽  
Sympathetic Nervous Activity ◽  
Urinary Catecholamine ◽  
Control Groups ◽  
Laboratory Staff ◽  
Metabolite Concentrations ◽  
Vanillyl Mandelic Acid ◽  
Sympathetic Nervous

1. Plasma noradrenaline concentrations were similar in normotensive and hypertensive outpatients, but were significantly lower in laboratory control subjects. 2. Standing plasma noradrenaline concentrations were similar in all three groups. 3. Urinary vanillyl mandelic acid, catecholamines and metanephrines were also similar in the normotensive and hypertensive groups. 4. Laboratory controls, possibly because of familiarity with the techniques of sphygmomanometry and blood sampling, may attain a ‘basal’ resting level of sympathetic nervous discharge more readily and rapidly than subjects who are unfamiliar with such procedures. 5. After orthostatic stimulation by standing for 2 min, the activity of the sympathetic nervous system, as determined by pulse rate and plasma noradrenaline concentrations, was similar in the three groups, despite the lower starting values in the laboratory staff. 6. The absence of differences in plasma noradrenaline or urinary catecholamine and metabolite concentrations does not support the hypothesis of excessive sympathetic nervous activity in essential hypertension.

Plasma catecholamines in pregnancy induced hypertension

1986 ◽  
Vol 71 (1) ◽  
pp. 111-115 ◽  
Author(s):  
Peter C. Rubin ◽  
Lucy Butters ◽  
Rosemary McCabe ◽  
John L. Reed
Keyword(s):  
Blood Pressure ◽  
Post Partum ◽  
Plasma Concentrations ◽  
Plasma Noradrenaline ◽  
Pregnancy Induced Hypertension ◽  
Noradrenaline Concentration ◽  
Induced Hypertension ◽  
Sympathetic Nervous ◽  
Noradrenaline And Adrenaline ◽  
In Pregnancy

1. Increased activity of the sympathetic nervous system has been implicated in the genesis of early hypertension in young people. Studies in pregnancy allow observations to be made on evolving, recently established and resolving hypertension in the human. We describe the results of two studies involving women who developed hypertension during pregnancy. 2. In the first study, plasma concentrations of noradrenaline and adrenaline were measured in 17 women with pregnancy induced hypertension (PIH) and 17 normotensive pregnant control subjects. Plasma noradrenaline (nmol/l) was lower in the PIH group compared with control patients in both semi-recumbent (1.11 ± 0.53 vs 1.98 ± 0.96, P < 0.001) and standing positions (1.31 ± 0.65 vs 2.57 ± 1.27, P < 0.005). Five days post partum, plasma noradrenaline had risen in the PIH group compared with pregnant values in semi-recumbent (1.65 ± 1.0 vs 1.11 ± 0.52, P < 0.05) and standing positions (2.46 ± 1.5 vs 1.31 ± 0.65, P < 0.05). In the normotensive patients plasma noradrenaline did not differ between post partum and pregnant values (1.51 ± 0.73 vs 1.98 ± 0.96 semi-recumbent; 2.00 ± 1.16 vs 2.57 ± 1.7 standing). 3. Logarithmic transformation of the noradrenaline concentration data resulted in a significant (P < 0.02) negative correlation with diastolic blood pressure in the pregnant patients but not post partum. Plasma adrenaline concentration was the same in both groups. 4. In the second study, plasma concentrations of noradrenaline and adrenaline were measured sequentially through pregnancy in five women who developed PIH and five control subjects who remained normotensive. There was no difference in catecholamine concentrations between groups at any stage, but noradrenaline concentration tended to fall as blood pressure rose in the PIH patients. 5. We conclude that the sympathetic nervous system does not contribute to the development of PIH but responds to the increased blood pressure with decreased activity.

Plasma Noradrenaline and Adrenaline in Patients with Thyrotoxicosis and Myxoedema

1973 ◽  
Vol 45 (2) ◽  
pp. 163-171 ◽  
Author(s):  
N. J. Christensen
Keyword(s):  
Venous Blood ◽  
Nervous Activity ◽  
Age Groups ◽  
Normal Subjects ◽  
Plasma Noradrenaline ◽  
Sympathetic Nervous Activity ◽  
Plasma Adrenaline ◽  
The Difference ◽  
Noradrenaline And Adrenaline ◽  
Hypothyroid Patients

1. Employing a precise and sensitive double-isotope derivative technique plasma noradrenaline and plasma adrenaline were measured in sixteen normal subjects, in eight patients with myxoedema and in ten patients with thyrotoxicosis. Venous blood was obtained while the subjects rested in the supine position. 2. In the normal subjects plasma noradrenaline averaged 0·22±SD 0·09 ng/ml and plasma adrenaline 0·05±SD 0·05 ng/ml. Plasma noradrenaline rose with increasing age. 3. In patients with myxoedema, plasma noradrenaline was increased approximately threefold. The difference between the normal subjects and the hypothyroid patients was more pronounced in the older age-groups. 4. Despite their elevated pulse rate patients with thyrotoxicosis showed significantly decreased plasma noradrenaline concentrations compared to the normal subjects. 5. In the hypothyroid and hyperthyroid subjects plasma adrenaline concentrations were not different from the values obtained in the normal subjects. 6. It is suggested that sympathetic nervous activity is decreased in thyrotoxicosis as a compensatory phenomenon to the direct effect of thyroid hormones on the cardiovascular system.

Postprandial Sympatho-Adrenal Activity: Its Relation to Metabolic and Cardiovascular Events and to Changes in Meal Frequency

1995 ◽  
Vol 89 (4) ◽  
pp. 349-357 ◽  
Author(s):  
Mario Vaz ◽  
Andrea Turner ◽  
Bronwyn Kingwell ◽  
Jaye Chin ◽  
Elizabeth Koff ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiovascular Events ◽  
Peak Plasma ◽  
Nervous Activity ◽  
Systolic Pressure ◽  
Plasma Noradrenaline ◽  
Whole Body ◽  
Sympathetic Nervous Activity ◽  
Insulin Levels ◽  
Sympathetic Nervous

1. Sympatho-adrenal activity was measured after the consumption of a 3.15 MJ mixed meal. Whole-body noradrenaline spillover rates, forearm plasma noradrenaline spillover and adrenaline secretion rates were derived using isotope dilution methodology. Heart rate and blood pressure spectral analysis measurements were also made. The relation of sympatho-adrenal activity to thermogenic and cardiovascular events was studied. Sympathetic nervous and thermogenic responses were measured for 120 min after the single 3.15 MJ meal and compared with those after three 1.05 MJ meals, given 30 min apart. 2. Whole-body and forearm plasma noradrenaline spillover, and the 0.1 Hz component of systolic pressure power all increased significantly postprandially, while the 0.1 Hz component of heart rate variability, an indirect index of cardiac sympathetic nervous activity, remained unaltered. Adrenaline secretion was unaltered postprandially. Whole-body plasma noradrenaline spillover and thermogenesis during the 120 min postprandial period were 37% and 36% higher after the single meal as compared with the multiple meals, although this was not statistically significant. 3. The sympathetic neural responses were delayed in relation to peak plasma insulin levels and sustained in the face of declining insulin levels. Energy expenditure increased significantly postprandially, but there was no direct quantitative relationship to plasma noradrenaline spillover. Forearm oxygen consumption did not increase postprandially despite significant increases in regional noradrenaline spillover. Thus, no close relation was demonstrated between postprandial sympathetic nervous activation and either insulin secretion or thermogenesis.

URINARY EXCRETION OF FREE CATECHOLAMINES IN GRAVES' DISEASE

1971 ◽  
Vol 49 (1) ◽  
pp. 167-173 ◽  
Author(s):  
R. I. S. BAYLISS ◽  
O. M. EDWARDS
Keyword(s):  
Urinary Excretion ◽  
Nervous Activity ◽  
Sympathetic Nervous Activity ◽  
Graves Disease ◽  
Apparent Increase ◽  
Catecholamine Excretion ◽  
Sympathetic Nervous ◽  
Noradrenaline And Adrenaline

SUMMARY As judged by the urinary excretion of free noradrenaline and adrenaline, the secretion of catecholamines is not increased in patients with Graves' disease. Catecholamine excretion was not reduced by treatment with propranolol or carbimazole singly or in combination. The possible mechanism in hyperthyroidism responsible for the apparent increase in sympathetic nervous activity and the mitigation of these features by propranolol is discussed.

scholarly journals Sympathetic Nervous Regulation in Patients with Cirrhosis: Pathogenesis of Fluid Retention and Formation of Ascites

1991 ◽  
Vol 5 (3) ◽  
pp. 103-111 ◽  
Author(s):  
Jens H Henriksen ◽  
Helmer Ring-Larsen ◽  
Niels Juel Christensen
Keyword(s):  
Portal Pressure ◽  
Nervous Activity ◽  
Plasma Renin ◽  
Fluid Retention ◽  
Plasma Noradrenaline ◽  
Sympathetic Nervous Activity ◽  
Arterial Blood ◽  
Regulatory Systems ◽  
Sympathetic Nervous ◽  
Arterial Blood Volume

Increased circulating noradrenaline in patients with cirrhosis is due to enhanced sympathetic nervous activity and is not merely the result of decreased clearance of catecholamines. There is a direct relation between the level of arterial norndrenaline and severity of cirrhosis, increased portal pressure and fluid accumulation; patients with the hepatorenal syndrome exhibit the highest values of plasma noradrenaline. In patients with cirrhosis, the kidneys have been identified as an important source of noradrenaline ‘spillover’ into plasma, which indicates enhanced sympathetic nervous activity in these organs. Moreover, the level of plasma noradrenaline is inversely related to renal bloodflow and urinary excretion of sodium, and directly related to plasma renin, vasopressin and aldosterone. An increased spillover of noradrenaline has recently been demonstrated in the splanchnic system and superior portosystemic collaterals. Reduced central and arterial blood volume and low arterial blood pressure secondary to peripheral vasodilation are probably important afferent stimuli for enhanced sympathetic nervous activity, although a nonvolume-dependent hepatic baroreceptor may also be present. The authors conclude that the sympathetic nervous system, in concert with other regulatory systems, plays an important role in sodium-water homeostasis and fluid retention, as well as in the systemic and hepatosplanchnic circulatory derangement seen in patients with cirrhosis.

Renin Release during Head-up Tilt Occurs Independently of Sympathetic Nervous Activity in Tetraplegic Man

1980 ◽  
Vol 59 (4) ◽  
pp. 251-256 ◽  
Author(s):  
C. J. Mathias ◽  
N. J. Christensen ◽  
H. L. Frankel ◽  
W. S. Peart
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Nervous Activity ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Activity ◽  
Plasma Noradrenaline ◽  
Sympathetic Nervous Activity ◽  
Head Up Tilt ◽  
Sympathetic Nervous

1. The role of the sympathetic nervous system in the release of renin during head-up tilt has been studied in five normal subjects and in four tetraplegic patients with cervical spinal-cord transection above the sympathetic outflow. Blood pressure, heart rate and concentrations of plasma noradrenaline, plasma adrenaline and plasma renin activity were measured during head-up tilt to 45° before and after acute β-adrenoreceptor blockade with intravenous propranolol. 2. In the normal subjects there were minimal changes in blood pressure during head-up tilt and there was a rise in both plasma noradrenaline concentration and plasma renin activity. After propranolol values of plasma renin activity at rest fell with little change occurring during head-up tilt. 3. In the tetraplegic patients there was a substantial fall in blood pressure during head-up tilt. Concentrations of plasma noradrenaline and adrenaline did not change but there was a marked increase in plasma renin activity. Values of plasma renin activity both at rest and during head-up tilt were unaffected by propranolol. 4. We conclude that in tetraplegic patients renin release during head-up tilt may occur independently of sympathetic nervous activity and is probably largely dependent on activation of renal vascular receptors.

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