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

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.

1981 ◽  
Vol 61 (5) ◽  
pp. 585-590 ◽  
Author(s):  
M. J. Brown ◽  
D. A. Jenner ◽  
D. J. Allison ◽  
C. T. Dollery

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.


1996 ◽  
Vol 14 (8) ◽  
pp. 951???960 ◽  
Author(s):  
Gavin W. Lambert ◽  
Mario Vaz ◽  
Chakravarthi Rajkumar ◽  
Helen S. Cox ◽  
Andrea G. Turner ◽  
...  

1995 ◽  
Vol 89 (4) ◽  
pp. 349-357 ◽  
Author(s):  
Mario Vaz ◽  
Andrea Turner ◽  
Bronwyn Kingwell ◽  
Jaye Chin ◽  
Elizabeth Koff ◽  
...  

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.


1991 ◽  
Vol 5 (3) ◽  
pp. 103-111 ◽  
Author(s):  
Jens H Henriksen ◽  
Helmer Ring-Larsen ◽  
Niels Juel Christensen

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.


1997 ◽  
Vol 20 (3) ◽  
pp. 149-156 ◽  
Author(s):  
Yoshiyuki Kawano ◽  
Osamu Tochikubo ◽  
Yasujiro Watanabe ◽  
Eiji Miyajima ◽  
Masao Ishii

1976 ◽  
Vol 51 (s3) ◽  
pp. 485s-488s ◽  
Author(s):  
H. M. Brecht ◽  
F. Banthien ◽  
W. Ernst ◽  
W. Schoeppe

1. Plasma noradrenaline was measured in fiftynine patients with mild to severe essential hypertension and in fifteen normotensive control subjects under basal and orthostatic conditions. 2. In patients with essential hypertension mean plasma noradrenaline concentrations were significantly higher than in control subjects under basal and orthostatic conditions. 3. In patients with essential hypertension basal diastolic blood pressure correlated closely with the corresponding plasma noradrenaline concentrations. 4. Long-term treatment with prindolol of patients with essential hypertension led to a significant fall in diastolic and systolic blood pressure and heart rate and to a significant decrease in plasma noradrenaline concentrations under basal and orthostatic conditions. 5. The adrenergic response to upright posture, reflected by an increase in plasma noradrenaline, was not abolished by prindolol. 6. It is concluded that the anti-hypertensive effect of prindolol in patients with essential hypertension is at least partially mediated by a decrease of sympathetic nervous activity.


1980 ◽  
Vol 59 (4) ◽  
pp. 251-256 ◽  
Author(s):  
C. J. Mathias ◽  
N. J. Christensen ◽  
H. L. Frankel ◽  
W. S. Peart

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.


2006 ◽  
Vol 114 (S 1) ◽  
Author(s):  
D Heutling ◽  
F Sayk ◽  
C Dodt ◽  
HL Fehm ◽  
A Hinney ◽  
...  

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