Cerebral metabolism and its relationship with sympathetic nervous activity in essential hypertension

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


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

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

1994 ◽  
Vol 1 ◽  
pp. 314
Author(s):  
E. Gotoh ◽  
T. Matsukawa ◽  
S. Sumita ◽  
K. Ashino ◽  
N. Takagi ◽  
...  

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.


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