Platelet aggregation, effects inhibitors

ACE inhibitors inhibit the degradation of bradykinin and potentiate the effects of bradykinin by about 50-100-fold. The prevention of bradykinin degradation by ACE inhibitors is particularly protective for the heart. Increased bradykinin levels prevent postischemic reperfusion arrhythmia, delays manifestations of cardiac ischemia, prevents platelet aggregation, and probably also reduces the degree of arteriosclerosis and the development of cardiac hypertrophy. The role of bradykinin and bradykinin-induced NO release for the improvement of cardiac functions by converting enzyme inhibitors has been demonstrated convincingly with use of a specific bradykinin receptor antagonist and inhibitors of NO-synthase. 

Anagrelide -inhibitor of platelet aggregation which causes thrombocytopenia -cardiovascular effects (CHF, edema, palpitations) -anemia -nausea and vomiting -headache... 

MAHMA NONOate spontaneously dissociates in a pH-dependent, first-order process with a half-life of 1 min at 37 °C. In vivo, examination in anesthetised rats showed, that MAHMA NONOate had both platelet inhibitory and vasodepressor effects [50]. Like other NONOates, MAHMA NONOate inhibited collagen-induced and ADP-induced rat platelet aggregation in a concentration-dependent manner [51]. ODQ, a soluble GS inhibitor, caused only small influence on the concentration-response curve to MAHMA NONOate, indicating that cGMP-independent mechanisms play a crucial role. A potential target of MAHMA NONOate induced inhibition was the sarco-endoplasmic reticulum calcium-ATPase of the platelet dense tubular system... 

A comprehensive, randomized, placebo-controlled trial of infused bolus L-arg and its enantiomer (D-arg) included healthy subjects, non-insulin dependent diabetics, hypertensive subjects, and normotensives with primary hypercholesterolemia [147]. A blood-pressure drop and an acute inhibition of ADP-induced aggregation in platelet-rich plasma were observed in all subjects after L-arg administration (<5 g). Both responses to L-arg infusion closely correlated in magnitude, were weaker in noninsulin dependent diabetics and hypercholesterolemics, and declined with increasing age. Notably, D-arg did not elicit any of the L-arg effects, which were reduced by some 70% when superimposed upon ongoing, nonselective NOS inhibition with infused L-N-monomethyl-arginine (L-NMMA). Since D-arg is not a NOS substrate, and L-NMMA is a substrate-competitive NOS inhibitor, the L-arg effects observed in this study were theorized to reflect a rise in vascular NO production by eNOS. In contrast, the inhibition of platelet aggregation observed in vitro after a 5 min L-arg infusion (160 mg total dose) into healthy subjects and patients with angiographic... 

An intravenous infusion of PAF causes rapid (within 60 s) intravascular platelet aggregation, thrombocytopenia and platelet factor 4 release, as well as a profound and reversible neutropenia, due to enhanced aggregation and adherence of these cells. In vitro, PAF effects on neutrophils are dependent upon extracellular Ca2+ and Mg2+ and occur within 60 s of addition. The addition of inhibitors of 5-lipoxygenase activity (e.g. ETYA, 5,8,11,14-eicosatetraenoic acid and NDGA, nordihydroguaiaretic acid) - but not those... 

Low doses of aspirin inhibit platelet aggregation and may be more effective than higher doses. Larger doses inhibit cyclooxygenase in arterial walls, interfering with prostacyclin production, a potent vasodilator and inhibitor of platelet aggregation. 

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