1987
DOI: 10.1016/0041-008x(87)90064-0
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Red blood cells generate nitric oxide from directly acting, nitrogenous vasodilators

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Cited by 68 publications
(17 citation statements)
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“…There was no spontaneous formation of NO; NO releasing-capacity followed the series: lOb = 10a 9b>12> Comparison of the data reported above with those of stimulation efficacy of the guanylate cyclase activity (E), shows a statistically significant degree of correlation, able to explain only 46.3% of variance (Equation 1; Coburn, 1987 (Ignarro et al, 1981;Kruszyna et al, 1987 port in favour of a NO-mediated, cyclic GMP-dependent mechanism of action. Some selected furoxan compounds showing the highest potency as vasodilators, also inhibit collagen-induced, human platelet aggregation.…”
Section: Formation Of Nitrite From Furoxansmentioning
confidence: 98%
“…There was no spontaneous formation of NO; NO releasing-capacity followed the series: lOb = 10a 9b>12> Comparison of the data reported above with those of stimulation efficacy of the guanylate cyclase activity (E), shows a statistically significant degree of correlation, able to explain only 46.3% of variance (Equation 1; Coburn, 1987 (Ignarro et al, 1981;Kruszyna et al, 1987 port in favour of a NO-mediated, cyclic GMP-dependent mechanism of action. Some selected furoxan compounds showing the highest potency as vasodilators, also inhibit collagen-induced, human platelet aggregation.…”
Section: Formation Of Nitrite From Furoxansmentioning
confidence: 98%
“…Azydek sodu ma także działanie rozkurczające na mięśnie gładkie obwodowych naczyń krwionośnych, co prowadzi do obniżenia ciś-nienia krwi. Metabolizm przebiega głównie w wą-trobie i OUN, następuje również jego przemiana do cyjanków [13] oraz do tlenku azotu w erytrocytach [27]. Szacuje się, że dawki doustne dla azydku sodu wynoszą 0,7-3,9 mg (dawki terapeutyczne obniża-jące ciśnienie krwi), 20-180 mg (dawki toksyczne), 700 mg -20 g (dawki śmiertelne) [26].…”
Section: Discussionunclassified
“…Sodium azide is mainly metabolized in the liver and CNS. It is also converted to cyanides [13] and to nitrogen oxide in erythrocytes [27]. It is estimated that oral doses of sodium azide are 0.7-3.9 mg (blood-pressure reducing therapeutic doses), 20-180 mg (toxic doses), 700 mg -20 g (lethal doses) [26].…”
Section: Discussionmentioning
confidence: 99%
“…Il inhiberait également de nombreuses autres metallo-enzymes (catalase, monooxygénase à cytochrome P450…). L'oxyde nitrique est, quant à lui, un puissant vasodilatateur [5,14].…”
Section: Discussionunclassified