Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.7.11.13 (
protein kinase C
)
49,245
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The in vitro effect of the histamine H(1)-receptor antagonist
Bromadryl
on aggregation of human blood platelets was studied.
Bromadryl
inhibited stimulated platelet aggregation in a dose-dependent way. Depending on the aggregation stimulus used, its mean inhibitory concentrations were 16 micromol/litre (thrombin), 18 micro mol/litre (A23187), 92 micromol/litre (adrenaline) and 395 micromol/litre (adenosine diphosphate). The inhibitory effect was most pronounced in aggregation stimulated with phorbol 12-myristate 13-acetate (IC(50) = 3 micromol/litre), suggesting interference of
Bromadryl
with
protein kinase C
activity. In
Bromadryl
-treated platelets, a very good correlation was found between aggregation and liberation of arachidonic acid; the correlation coefficients calculated for thrombin- and A23187-stimulated platelets were 0.94123 and 0.98611, respectively. This indicates that interaction of
Bromadryl
with phospholipase A(2) (an enzyme liberating arachidonic acid) may be involved in the anti-aggregatory effect. However, in platelets stimulated with thrombin, thromboxane formation was decreased at a lower mean inhibitory concentration of
Bromadryl
(6 micromol/litre) than arachidonic acid liberation (72 micromol/litre); thus, phospholipase A(2) does not seem to be the only site in the arachidonate metabolism cascade affected by
Bromadryl
. Although specific interference of
Bromadryl
with histamine receptors could not be excluded, alterations in platelet membrane structure and functions are supposed to be principal in the anti-aggregatory effect of
Bromadryl
.
...
PMID:Decreased arachidonic acid liberation participates in the anti-aggregatory effect of the histamine H(1)-receptor antagonist Bromadryl. 1680 Nov 18
