An Electrochemical Engineering Perspective of Nitric Oxide in Tumors: Why the Combination of an Allosteric Effector of Hemoglobin with Dietary Sodium Nitrite Should Be Effective in Treating Vascularized Tumors?

2019 ◽  
Vol 28 (33) ◽  
pp. 1-6
Author(s):  
Adam Heller
Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Lucas C Pinheiro ◽  
Jefferson H Amaral ◽  
Carla S Ceron ◽  
Graziele Ferreira ◽  
Jose E Tanus-Santos

Introduction: Recent studies showed that sodium nitrite decreases blood pressure (BP) in two kidney, one clip (2K1C) hypertension, probably as a result of nitrite being converted into nitric oxide in the acid environment of the stomach. This study aimed at examining whether increasing gastric pH with omeprazol reduces the chronic antihypertensive effects of nitrite. Methods: 2K1C hypertensive and sham operated control rats were treated with omeprazole (10mg/Kg; i.p.) or vehicle and sodium nitrite (15mg/Kg; gavage) or saline for two weeks. Systolic BP (SBP) was measured by tail pletismografy weekly. Circulating nitrite levels were measured by chemiluminesce and gastric pH was measured with an electrode. The results were analyzed by two-way ANOVA. The results are show as mean ± standard deviation. Results: 2K1C rats were hypertensive two weeks after surgery (SBP=180±17 mmHg). After 4 weeks of treatment, nitrite exerted antihypertensive effects in rats treated with vehicle (SBP=161±23 mmHg versus 200±29 mmHg, respectively, in the 2K1C+nitrite and in the 2K1C+saline groups; P<0.05). However, nitrite exerted no antihypertensive effects in 2K1C rats treated with omeprazole (SBP=200±34 mmHg; P>0.05 versus 2K1C+saline group). We found no significant differences among the sham operated groups. Similar increases in plasma nitrite concentrations were found when animals treated with nitrite and omeprazol were compared with those treated with nitrite and vehicle (8.5±4.1 versus 5.2±3.6 μM, respectively; P>0.05). Omeprazole increased gastric pH in all animals treated with this drug (P<0.05). Conclusion Treatment with omeprazole blunts the chronic antihypertensive effects of sodium nitrite in 2K1C rats. However, this effect is probably not associated with significant differences in plasma nitrite concentrations.


2005 ◽  
Vol 22 (Supplement 36) ◽  
pp. 17
Author(s):  
M. J. Souter ◽  
J. D. Moulding ◽  
S. Deem ◽  
D. An ◽  
A. A. Artru

2021 ◽  
Vol 67 (6) ◽  
pp. 404-416
Author(s):  
Motoko OARADA ◽  
Yuushi OKUMURA ◽  
Katsuya HIRASAKA ◽  
Kosuke SUGIURA ◽  
Nobuhiko TACHIBANA ◽  
...  

2017 ◽  
Vol 95 (4) ◽  
pp. 447-454 ◽  
Author(s):  
Vivien Demeter-Haludka ◽  
László Juhász ◽  
Mária Kovác ◽  
János Gardi ◽  
Ágnes Végh

This study aimed to examine whether inducible nitric oxide synthase (iNOS) plays a role in the delayed antiarrhythmic effect of sodium nitrite. Twenty-one dogs were infused intravenously with sodium nitrite (0.2 μmol·kg–1·min–1) for 20 min, either in the absence (n = 12) or in the presence of the iNOS inhibitor S-(2-aminoethyl)-isothiourea (AEST) (total dose 2.0 mg·kg–1 i.v., n = 9). Control dogs (n = 12) were given saline. Twenty-four hours later, all of the dogs were subjected to a 25 min period occlusion of the left anterior descending coronary artery followed by rapid reperfusion. Dogs treated with AEST and nitrite received again AEST prior to the occlusion. Compared with the controls, sodium nitrite markedly reduced the number of ectopic beats, the number and incidence of ventricular tachycardia, and the incidence of ventricular fibrillation during occlusion and increased survival (0% versus 50%) from the combined ischaemia and reperfusion insult. Although AEST completely inhibited iNOS activity, the nitrite-induced increase in NO bioavailability during occlusion was not substantially modified. Furthermore, AEST attenuated but did not completely abolish the antiarrhythmic effect of nitrite. The marked delayed antiarrhythmic effect of sodium nitrite is not entirely due to the activation of iNOS; other mechanisms may certainly play a role.


Hypertension ◽  
1996 ◽  
Vol 27 (3) ◽  
pp. 688-692 ◽  
Author(s):  
David L. Mattson ◽  
Daniel J. Higgins

e-Polymers ◽  
2002 ◽  
Vol 2 (1) ◽  
Author(s):  
Christophe Detrembleur ◽  
Ange Mouithys-Mickalad ◽  
Philippe Teyssié ◽  
Robert Jérôme

AbstractA mixture of sodium nitrite and ascorbic acid is able to control the radical polymerization of tert-butyl methacrylate (tBMA) in water at 80°C. Indeed, sodium nitrite is reduced by the ascorbic acid, and the nitric oxide (NO) which is formed insitu is nothing but a promoter of nitroxyl radicals. The radical polymerization of tBMA is thus basically controlled by a nitroxide-mediated process.


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