Lowering of Blood Pressure Improves Endothelial Dysfunction by Increase of Nitric Oxide Production in Hypertensive Rats.

We determined erythrocyte physiological and biochemical properties after the single and repeated administration of ultra-small superparamagnetic iron-oxide nanoparticles (USPIONs) in normotensive Wistar–Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Polyethylene glycol-coated USPIONs (transmission electron microscope detected a mean size of ~30 nm and hydrodynamic size ~51 nm) were intravenously administered to rats either in one infusion at nominal dose 1 mg Fe/kg or in two infusions (administered with a difference of 24 h) at nominal dose 2 mg Fe/kg. Results showed that USPIONs did not deteriorate erythrocyte deformability, nitric oxide production, and osmotic resistance in both experimental settings. Both the single and repeated USPION administration elevated erythrocyte deformability in WKY. However, this effect was not present in SHR; deformability in USPION-treated SHR was significantly lower than in USPION-treated WKY. Nitric oxide production by erythrocytes was increased after a single USPION treatment in WKY, so it can be associated with improvement in erythrocyte deformability. Using biomagnetometry, we revealed significantly lower amounts of USPION-originated iron in erythrocytes in SHR compared with WKY. We found a much faster elimination of USPIONs from erythrocytes in hypertensive rats compared with the normotensive ones, which might be relevant for clinical practice in hypertensive patients undergoing clinical examination with the use of iron-oxide nanoparticles.

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Antioxidant treatment normalizes nitric oxide production, renal sodium handling and blood pressure in experimental hyperleptinemia

Life Sciences ◽

10.1016/j.lfs.2005.02.013 ◽

2005 ◽

Vol 77 (15) ◽

pp. 1855-1868 ◽

Cited By ~ 12

Author(s):

Jerzy Beltowski ◽

Grażyna Wójcicka ◽

Anna Jamroz-Wiśniewska ◽

Ewelina Borkowska ◽

Andrzej Marciniak

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Nitric Oxide Production ◽

Antioxidant Treatment ◽

Oxide Production ◽

Renal Sodium Handling ◽

Sodium Handling

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Brain nitric oxide production by a proline-rich decapeptide from Bothrops jararaca venom improves baroreflex sensitivity of spontaneously hypertensive rats

Hypertension Research ◽

10.1038/hr.2010.208 ◽

2010 ◽

Vol 33 (12) ◽

pp. 1283-1288 ◽

Cited By ~ 10

Author(s):

Claudiana Lameu ◽

Vera Pontieri ◽

Juliano R Guerreiro ◽

Eduardo F Oliveira ◽

Carlos Alberto da Silva ◽

...

Keyword(s):

Nitric Oxide ◽

Spontaneously Hypertensive Rats ◽

Baroreflex Sensitivity ◽

Nitric Oxide Production ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Oxide Production ◽

Bothrops Jararaca ◽

Brain Nitric Oxide

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Exaggerations in skeletal muscle metaboreflex activity are attenuated by increasing nitric oxide production within the brainstem of spontaneously hypertensive rats

The FASEB Journal ◽

10.1096/fasebj.23.1_supplement.608.1 ◽

2009 ◽

Vol 23 (S1) ◽

Author(s):

Anna K Leal ◽

Jere H Mitchell ◽

Scott A Smith

Keyword(s):

Nitric Oxide ◽

Skeletal Muscle ◽

Spontaneously Hypertensive Rats ◽

Nitric Oxide Production ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Muscle Metaboreflex ◽

Oxide Production

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POSSIBLE WAYS OF STIMULATION OF NITRIC OXIDE PRODUCTION AS THE MAIN INDUCTOR OF ENDOTHELIAL DYSFUNCTION USING CARDIOTROPIC DRUGS IN PATIENTS WITH PERIPHERAL OCCLUSIVE ARTERIAL DISEASE

I P Pavlov Russian Medical Biological Herald ◽

10.17816/pavlovj201128-8 ◽

2011 ◽

Vol 19 (2) ◽

pp. 8 ◽

Cited By ~ 1

Author(s):

Pavel Grigor'evich Shval'b ◽

Roman Evgen'evich Kalinin ◽

Aleksandr Sergeevich Pshennikov ◽

P G Shvalb ◽

R E Kalinin ◽

...

Keyword(s):

Nitric Oxide ◽

Endothelial Dysfunction ◽

Arterial Disease ◽

Nitric Oxide Production ◽

Peripheral Occlusive Arterial Disease ◽

Occlusive Arterial Disease ◽

Oxide Production ◽

Cardiotropic Drugs ◽

Stimulation Of

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

Hypertension ◽

10.1161/hypertensionaha.119.14636 ◽

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.

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