Effects of elevated plasma noradrenaline concentration on the immune system in humans

1998 ◽  
Vol 79 (1) ◽  
pp. 93-98 ◽  
Author(s):  
M. Kappel ◽  
T. D. Poulsen ◽  
H. Galbo ◽  
B. K. Pedersen
2006 ◽  
Vol 130 (1-2) ◽  
pp. 65
Author(s):  
Naoko Sumita ◽  
Naotoshi Tamura ◽  
Toshimasa Yamamoto ◽  
Kunio Shimazu

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

1981 ◽  
Vol 61 (s7) ◽  
pp. 165s-168s ◽  
Author(s):  
A. M. M. Shepherd ◽  
M.-S. Lin ◽  
T. K. Keeton ◽  
J. L. McNay

1. Changes in plasma noradrenaline levels and heart rate were used as measures of baroreflex sensitivity in six hypertensive subjects given serial incremental doses of sodium nitroprusside (intravenously) to lower blood pressure. 2. The rises in both heart rate and plasma noradrenaline concentration were linearly related to the decrement in blood pressure and inversely related to the severity of the hypertension. 3. A positive correlation between rise in heart rate and rise in plasma noradrenaline was found for each subject. With increasing severity of hypertension, a greater increase in heart rate occurred for each increment in plasma noradrenaline concentration. 4. Baroreflex sensitivity can be assessed by relating changes in heart rate to change in arterial pressure; however, this method does not distinguish the relative contributions of the vagal and sympathetic components of the autonomic neural response or variations in the chronotropic response to sympathetic stimulation. 5. Changes in plasma noradrenaline levels in response to graded reductions in blood pressure may be a more appropriate measure of baroreflex sensitivity than the methods currently used in clinical investigation.


1980 ◽  
Vol 59 (s6) ◽  
pp. 311s-313s ◽  
Author(s):  
M. Esler ◽  
G. Jackman ◽  
P. Leonard ◽  
A. Bobik ◽  
Helen Skews ◽  
...  

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.


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