scholarly journals Effect of MnSOD (E. coli) on the relaxation caused by sodium nitroprusside on isolated rat renal artery

2004 ◽  
Vol 69 (11) ◽  
pp. 973-980 ◽  
Author(s):  
Slobodan Milovanovic ◽  
Zorana Orescanin ◽  
Snezana Spasic ◽  
Srdjan Miletic ◽  
Milica Prostran ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Artery ◽  
Sodium Nitroprusside ◽  
Relaxation Effect ◽  
Renal Arteries ◽  
Nitric Oxide Donor ◽  
No Production ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Relaxation Effects

In this study themolecular foundation of nitric oxide induced relaxation of arteries, with or without endothelium, of normotensive and spontanously hypertensive ratswas re-examined. With this purpose in mind, the effects of the nitric oxide donor sodium nitroprusside (NaNP), with and without manganese containing superoxide dismutase (MnSOD E.C. 1.15.1.1), on rat renal artery relaxation was strudied. The results show that the relaxation effect of NaNP is two times higher in normotensive, compared to spontaneously hypertensive rats. Similar differences exist in the relaxation effects of NaNP on isolated renal arteries without endothelium, indicating that besides the difference in the function of an endothelium, concerning basal NO production in normotensive and hypertensive rats, there is a differencewith respect to NO relaxation in the smoothmuscle that is induced by hypertension. MnSOD decreased the relaxation effect of NaNP in all the examined renal arteries, more in normotensive than in hypertensive ones regardless of the presence of an endothelium. These results show that MnSOD, by modifying the chemical versatility of NO into redox active forms - nitrosonium (NO+) and nitroxyl (NO-), produces different relaxation effects in normotensive and hypertensive arteries of rats, with or without an endothelium, potentiating the role of nitroxyl induced relaxation in sponteneously hypertensive rats. The results prove the need for the synthesis of complex NO donors, as the mechanisms of artery relaxation are different due to an endothel and smooth mouscle changes in hypertensive, as compared to normotensive rats.

scholarly journals Endothelial modulation of a nitric oxide donor complex-induced relaxation in normotensive and spontaneously hypertensive rats

Life Sciences ◽  
2018 ◽  
Vol 201 ◽  
pp. 130-140 ◽  
Author(s):  
Simone R. Potje ◽  
Jéssica A. Troiano ◽  
Marcella D. Grando ◽  
Murilo E. Graton ◽  
Roberto S. da Silva ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Spontaneously Hypertensive Rats ◽  
Nitric Oxide Donor ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

scholarly journals Perindoprilat Changes ANG (1-9) Production in Renal Arteries Isolated From Young Spontaneously Hypertensive Rats After ANG I Incubation

2016 ◽  
pp. 561-570
Author(s):  
P. P. WOŁKOW ◽  
B. BUJAK-GIŻYCKA ◽  
J. JAWIEŃ ◽  
R. OLSZANECKI ◽  
J. MADEJ ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Renal Artery ◽  
Spontaneously Hypertensive Rats ◽  
Renal Arteries ◽  
Ang Ii ◽  
Shr Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Old Rats ◽  
Wistar Kyoto

We used mass spectrometry to quantitate production of angiotensinogen metabolites in renal artery of 3- and 7-month-old Wistar-Kyoto (WKY) and Spontaneously Hypertensive Rats (SHR). Tissue fragments were incubated for 15 min in oxygenated buffer, with added angiotensin I. Concentrations of angiotensins I (ANG I), II (ANG II), III (ANG III), IV (ANG IV), angiotensin (1-9) [ANG (1-9)], angiotensin (1-7) [ANG (1-7)], and angiotensin (1-5) [ANG (1-5)], excreted into the buffer during experiment, were measured using liquid chromatography-mass spectrometry (LC/MS) and expressed per mg of dry tissue. Effects of pretreatment with 10 μM perindoprilat on the production of ANG I metabolites were quantitated. Background production of any of ANG I metabolites differed neither between WKY and SHR rats nor between 3- and 7-month-old rats. Perindoprilat pretreatment of renal arteries resulted, as expected, in decrease of ANG II production. However, renal arteries of 7-month-old SHR rats were resistant to ACE inhibitor and did not change ANG II production in response to perindoprilat. In renal arteries, taken from 3-month-old rats, pretreated with perindoprilat, incubation with ANG I, resulted in the level of ANG (1-9) significantly higher in SHR than WKY rats. Our conclusion is that in SHR rats, sensitivity of renal artery ACE to perindoprilat inhibition changes with age.

scholarly journals Increased Blood Pressure Causes Lymphatic Endothelial Dysfunction via Oxidative Stress in Spontaneously Hypertensive Rats

Hypertension ◽  
2020 ◽  
Vol 76 (2) ◽  
pp. 598-606
Author(s):  
Masashi Mukohda ◽  
Risuke Mizuno ◽  
Hiroshi Ozaki
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Nadph Oxidase ◽  
Sodium Nitroprusside ◽  
P38 Mapk ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

The lymphatic system is involved in the pathogenesis of edema, inflammation, and cancer metastasis. Because lymph vessels control fluid electrolytes and volume balance, changes in lymphatic activity can be expected to alter systemic blood pressure. This study examined possible changes in lymphatic contractile properties in spontaneously hypertensive rats (SHR). Thoracic ducts isolated from 10- to 12-week-old SHR exhibited either decreased acetylcholine-induced endothelium-dependent relaxation or sodium nitroprusside-induced endothelium-independent relaxation compared with age-matched Wister-Kyoto rats. The impairment in acetylcholine responsiveness was more pronounced than sodium nitroprusside responsiveness. N-Nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor blunted acetylcholine-induced relaxation in Wister-Kyoto rats, indicating an involvement of endothelial nitric oxide production. Endothelial dysfunction in lymph vessels of SHR was attenuated by tempol (a superoxide dismutase mimetic), apocynin, or VAS-2870 (NADPH oxidase inhibitors). Consistent with these observations, nitrotyrosine levels were significantly elevated in SHR, indicative of increased oxidative stress. In addition, protein expression of NADPH oxidase 2 and phosphorylation of p47 phox (Ser345) were significantly increased in SHR. Further, SB203580 (a p38 MAPK inhibitor) restored the acetylcholine-induced relaxation in SHR. It is notable that 4-week-old SHR, which exhibited normal blood pressure, did not show any decreased activity of acetylcholine- or sodium nitroprusside-induced relaxation. Additionally, antihypertensive treatment of 4-week-old SHR with hydrochlorothiazide and reserpine or hydrochlorothiazide and hydralazine for 6 weeks completely restored lymphatic endothelial dysfunction. We conclude that contractile activity of lymphatic vessels is functionally impaired with the development of increasing blood pressure, which is mediated through increased oxidative stress via the p38 MAPK/NADPH oxidase 2 pathway.

scholarly journals The new nitric oxide donor 2-nitrate-1,3-dibuthoxypropan alters autonomic function in spontaneously hypertensive rats

2012 ◽  
Vol 171 (1-2) ◽  
pp. 28-35 ◽  
Author(s):  
Maria S. França-Silva ◽  
Matheus M.O. Monteiro ◽  
Thyago M. Queiroz ◽  
Alexsandro F. Santos ◽  
Petrônio F. Athayde-Filho ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Spontaneously Hypertensive Rats ◽  
Autonomic Function ◽  
Nitric Oxide Donor ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

scholarly journals Nebivolol combined with tetrahydrobiopterin affects diastolic function in spontaneously hypertensive rats via the nitric oxide/cyclic guanosine monophosphate signalling pathway

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Xiaoli Guan ◽  
Xiaoying Guan ◽  
Changhong Lu ◽  
Bo Shang ◽  
Yuan Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Diastolic Dysfunction ◽  
Spontaneously Hypertensive Rats ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
No Production ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Myocardial Oxidative Stress

Abstract Background Hypertension is the the primary cause of diastolic heart failure. Oxidative stress plays an important role in cardiac diastolic dysfunction caused by hypertension. The occurrence of oxidative stress is related to the level of nitric oxide (NO) in the body. Tetrahydrobiopterin (BH4) is an essential cofactor for NO synthesis. Nebivolol can reduce myocardial oxidative stress and increase NO activity. Therefore, we investigated the effects of monotherapy or combination therapy of different doses of BH4 and nebivolol on cardiac diastolic function in spontaneously hypertensive rats, and preliminarily expounded the related mechanisms. Methods Left ventricular function was evaluated by non-invasive echocardiographic assessment and invasive right carotid artery catheterization methods. ELISA was used to measure myocardial 3-nitrotyrosine content, NO production, and cyclic guanosine monophosphate (cGMP) concentration in the myocardium; quantitative real-time PCR (qRT-PCR) was used to determine endothelial nitric oxide synthase (eNOS), phospholamban and sarcoplasmic reticulum Ca2+-ATPase 2a (SERCA2a) mRNA expression levels; Western blot was used to detect the protein expression levels of eNOS and eNOS dimers in myocardial tissue, and immunohistochemical detection of cGMP expression in the myocardium was performed. Results Studies have shown that compared with those in the control group, NO generation and the expression level of myocardial eNOS mRNA, eNOS expression of dimers, phospholamban, SERCA2a and cGMP increased significantly after the combined intervention of BH4 and nebivolol, while the expression of 3-nitrotyrosine was significantly decreased. Conclusions The combined treatment group had a synergistic effect on reducing myocardial oxidative stress, increasing eNOS content, and increasing NO production, and had a more obvious protective effect on diastolic dysfunction through the nitric oxide/cyclic guanosine monophosphate (NO/cGMP) pathway.

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