{'fraction_non_alphanumeric': 0.03292568203198495, 'fraction_numerical': 0.004703668861712135, 'mean_word_length': 6.046357615894039, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Antiplatelet effects of endothelium-derived relaxing factor and nitric oxide donors.

Several circulating agonists and hydromechanical factors, such as the viscous drag-induced shear forces of the blood stream, stimulate the release of endothelium-derived relaxing factor (EDRF) or nitric oxide (NO) from endothelial cells. Abluminally released EDRF controls vascular tone, while luminally released EDRF diffuses into the platelets, especially when they come into close contact with the endothelial cell lining. Stimulation of soluble guanylyl cyclase in platelets causes a rise in cyclic 3',5'-guanosine monophosphate (cGMP) and a reduction in intracellular Ca(2+)-concentrations. This suppresses platelet adhesion and aggregation and potentiate similar prostacylin-induced rises in cyclic 3',5'-adenosine monophosphate. Nitrovasodilators, which spontaneously release NO, such as molsidomine and sodium nitroprusside, can act as a substitute for diminished EDRF release from deficient endothelium and similarly suppress platelet aggregation in vitro and in vivo.