Biochemical and Biophysical Research Communications
Regular ArticleInhibition of Platelet Adhesion to Collagen by cGMP-Elevating Agents
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2019, Biochemical PharmacologyCitation Excerpt :Dipyridamole (2,6–bis (diethanolamino)–4,8-dipiperidino-pyrimido 5,4-d pyrimidine), synthesized more than fifty years ago and initially used as a coronary vasodilator, inhibits platelet aggregation by acting on multiple targets, and namely by inhibiting the reuptake of adenosine by RBC [108] thus enhancing the circulating levels of this nucleoside which exerts an antiplatelet activity by stimulating platelet adenylylcycalse, by inhibiting PDE5 and PDE3, and by acting as a antioxidant [107]. Dipyridamole potentiates the inhibitory effects of NO on human platelets by inhibiting PDE5, thus enhancing NO-stimulated intraplatelet cGMP [109], enhances the platelet adhesion-suppressing effect of cGMP-elevating agents [110], potentiates the antiplatelet effects of aspirin in whole blood or in the presence of white blood cells [108] and increases cGMP-mediated platelet VASP phosphorylation confirming the preeminent role of NO in its action [111]. Dipyridamole potentiated the beneficial effects of adenosine on ischemia/reperfusion damage-induced myocardial dysfunction in guinea pigs by inhibiting platelet adhesion [112] and strongly potentiated the antithrombotic properties of inhaled NO in a canine model of platelet-mediated coronary artery thrombosis without prolonging the bleeding time [113].
Neuroprotective potential of high-dose biotin
2017, Medical HypothesesCitation Excerpt :All of the rats who received saline without biotin experienced strokes, whereas none in the biotin group did; mortality in the former group was 40%, but none of the biotin-treated rats died. It is well known that NO exerts a stabilizing effect on platelets, and also inhibits their adhesion to collagen; this effect is known to be mediated by cGMP [76–78]. It is therefore reasonable to suspect that high-dose biotin could likewise stabilize platelets; potentially this phenomenon might have contributed to the absence of stroke in the biotin-treated hypertensive rats.
YC-1 potentiates cAMP-induced CREB activation and nitric oxide production in alveolar macrophages
2012, Toxicology and Applied PharmacologyCitation Excerpt :3-(5′-Hydroxymethyl-2′-furyl)-1-benzyl indazole (YC-1), an NO-independent and heme-dependent sGC activator, also sensitizes sGC to NO and carbon monoxide (CO) (Friebe et al., 1996, 1998; Ko et al., 1994). Through activation of sGC, YC-1 shows versatile pharmacological functions including inhibiting platelet aggregation and adhesion (Friebe et al., 1998; Wu et al., 1995, 1997), as well as decreasing vascular smooth muscle proliferation and contractions (Mulsch et al., 1997; Tulis, 2008). However, several studies showed that YC-1 exhibits several additional effects that do not involve the sGC/cGMP pathway.
YC-1 attenuates homotypic human neutrophil aggregation through inhibition of phosphodiesterase activity
2008, European Journal of PharmacologyMeasurement of adhesion of human platelets in plasma to protein surfaces in microplates
2005, Journal of Pharmacological and Toxicological MethodsControl of platelet activation by cyclic AMP turnover and cyclic nucleotide phosphodiesterase type-3
2004, Biochemical PharmacologyCitation Excerpt :In combination with SNP, general PDE inhibition (papaverine) and PDE5 inhibition (dipyridamole, zaprinast, sildenafil) further raised the cGMP level, with zaprinast and sildenafil being most active. A similar, minor increase in cGMP by dipyridamole alone but high increase upon simultaneous guanylate cyclase activation has also been observed by others [29]. Typically, the type-3/4 inhibitor zardaverine also caused cGMP elevation in this case.
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Address for correspondence: Dr. Che-Ming Teng, Pharmacological Institute, College of Medicine, National Taiwan University, No. 1, Jen-Ai Rd., 1st Section, Taipei, 10018, Taiwan. Fax: 886-2-322-1742.