Effect of inhibitors of catecholamine synthesis (?-methyltyrosine and disulfiram) on spontaneous unit activity of the sensomotor cortex and responses to afferent, caudate, and reticular stimulation

1974 ◽  
Vol 78 (3) ◽  
pp. 1023-1026
Author(s):  
�. B. Arushanyan ◽  
Yu. A. Belozertsev
1981 ◽  
Vol 6 (2) ◽  
pp. 151-154 ◽  
Author(s):  
V. Rettori ◽  
A. Seilicovich ◽  
S. Goijman ◽  
L. Debeljuk

1973 ◽  
Vol 4 (2) ◽  
pp. 85-90
Author(s):  
�. B. Arushanyan ◽  
Yu. A. Belozertsev

1988 ◽  
Vol 60 (02) ◽  
pp. 251-254 ◽  
Author(s):  
S E Kjeldsen ◽  
K Gjesdal ◽  
P Leren ◽  
I K Eide

SummaryThe content of free-catecholamines in blood platelets is much higher than in plasma and platelet catecholamines must be taken up from plasma, since platelets lack the enzymes for catecholamine synthesis. There is some evidence that platelet catecholamine content under certain circumstances may be an integrated measure of plasma catecholamine concentrations over time. Platelet-free catecholamines were therefore assayed in 18 untreated patients with essential hypertension and in 16 normotensive control subjects. Mean platelet-free dopamine in the hypertensive group was 3.7 ± 0.4 pg/mg platelet weight, i.e. significantly less than the 6.5 ± 0.9 pg/mg found in the normotensive (p <0.005). Platelet contents of noradrenaline and adrenaline did not differ. Decreased platelet-free dopamine and unchanged platelet noradrenaline and adrenaline persisted after adjustment for increased body weight in the hypertensive group. Although the reasons for decreased platelet-free dopamine in the hypertensive group remain unknown, this finding may add to previous result showing facilitated release of granular contents from blood platelets in patients with essential hypertension. Our data do not support platelet levels of free-catecholamines to be a marker of increased sympathetic tone in essential hypertension.


1973 ◽  
Vol 29 (03) ◽  
pp. 633-643
Author(s):  
H Gjønnæss

SummaryThe cold promoted activation of factor VII occurs in parallel with an activation of a plasma arginine esterase, and, on inhibition of the cold activation of factor VII, the esterase activation also decreased. The inhibitor pattern supported our theory that the arginine esterase that is activated in the cold activation of factor VII is plasma kallikrein.The cold activation of factor VII was completely inhibited with soya bean trypsin inhibitor in doses that did not interfere with the contact activation. On the other hand, inhibition of the contact activation with hexadimethrine bromide did not interfere with the cold activation of factor VII except when this was kaolin induced. Contact and cold activation therefore appear to represent two different pathways for the activation of factor VII. The cold activation reaction is probably mediated by the activation of plasma prekallikrein, and inhibition of the plasma kallikrein activity correlates with the inhibition of the cold promoted activation of factor VII.


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