1974 ◽  
Vol 46 (4) ◽  
pp. 481-488 ◽  
Author(s):  
C. S. Wilcox ◽  
M. J. Aminoff ◽  
A. B. Kurtz ◽  
J. D. H. Slater

1. The effect on plasma renin activity (PRA) of dopamine and noradrenaline infusions was studied in three patients with Shy—Drager syndrome, three patients with Parkinson's disease and normal autonomic reflexes, and three healthy volunteers. The patients with the Shy—Drager syndrome had functional evidence of a peripheral lesion of the sympathetic nervous system and subnormal PRA on a controlled sodium intake. 2. In all subjects catecholamines were infused step-wise for 4 min until a 30% rise in systolic blood pressure occurred. 3. In each subject, PRA fell after noradrenaline but rose after dopamine. The mean fractional increase in PRA after dopamine was no less in the Shy—Drager patients than in the control groups. 4. The results suggest, first, that stimulation of dopamine receptors can release renin, and secondly, that inadequate renin stores cannot explain the low PRA found in our patients with autonomic failure.


1995 ◽  
Vol 99 (6) ◽  
pp. 604-610 ◽  
Author(s):  
Fetnat M. Fouad-Tarazi ◽  
Masanori Okabe ◽  
Hershel Goren

1974 ◽  
Vol 34 (3) ◽  
pp. 288-294 ◽  
Author(s):  
M.Mohsen Ibrahim ◽  
Robert C. Tarazi ◽  
Harriet P. Dustan ◽  
Emmanuel L. Brav

2003 ◽  
Vol 6 (4) ◽  
pp. 170-177
Author(s):  
Ina E. Djonlagic ◽  
Jeffrey A. Cohen

Heart Rhythm ◽  
2005 ◽  
Vol 2 (5) ◽  
pp. S111
Author(s):  
Yousef Kanjwal ◽  
Daniel Kosinski ◽  
George Maly ◽  
Mark Kligman ◽  
Blair P. Grubb

2010 ◽  
Vol 3 (130) ◽  
pp. ec213-ec213
Author(s):  
N. R. Gough

1982 ◽  
Vol 142 (2) ◽  
pp. 339-344 ◽  
Author(s):  
W. L. Henrich

Author(s):  
Karl E. Misulis ◽  
E. Lee Murray

Autonomic difficulty is usually a component of a systemic disease with other neurologic manifestations. A commonality is orthostatic hypotension for most of these. Once the diagnosis of autonomic insufficiency has been made, the differential diagnosis includes disorders described in this chapter.


1982 ◽  
Vol 142 (2) ◽  
pp. 339 ◽  
Author(s):  
William L. Henrich

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.


Sign in / Sign up

Export Citation Format

Share Document