Role of Nitric Oxide in the Evolution of Renal Ischemia in Two-Kidney, One-Clip Renovascular Hypertension.

Although Acanthospermum hispidum is used in Brazilian folk medicine as an antihypertensive, no study evaluated its effects on a renovascular hypertension and ovariectomy model. So, this study investigated the mechanisms involved in the antihypertensive effects of an ethanol-soluble fraction obtained from A. hispidum (ESAH) using two-kidney-one-clip hypertension in ovariectomized rats (2K1C plus OVT). ESAH was orally administered at doses of 30, 100, and 300 mg/kg, daily, for 28 days, after 5 weeks of surgery. Enalapril (15 mg/kg) and hydrochlorothiazide (25 mg/kg) were used as standard drugs. Diuretic activity was evaluated on days 1, 7, 14, 21, and 28. Systolic, diastolic, and mean blood pressure and heart rate were recorded. Serum creatinine, urea, thiobarbituric acid reactive substances, nitrosamine, nitrite, aldosterone, vasopressin levels, and ACE activity were measured. The vascular reactivity and the role of nitric oxide (NO) and prostaglandins (PG) in the vasodilator response of ESAH on the mesenteric vascular bed (MVB) were also investigated. ESAH treatment induced an important saluretic and antihypertensive response, therefore recovering vascular reactivity in 2K1C plus OVT-rats. This effect was associated with a reduction of oxidative and nitrosative stress with a possible increase in the NO bioavailability. Additionally, a NO and PG-dependent vasodilator effect was observed on the MEV.

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The role of nitric oxide pathway in the renal ischemia–reperfusion injury in rats

Transplant Immunology ◽

10.1016/s0966-3274(02)00079-5 ◽

2002 ◽

Vol 10 (4) ◽

pp. 277-284 ◽

Cited By ~ 28

Author(s):

Ernani Luı́s Rhoden ◽

Cláudia Ramos Rhoden ◽

Márcio Luı́s Lucas ◽

Luiz Pereira-Lima ◽

Cláudio Zettler ◽

...

Keyword(s):

Nitric Oxide ◽

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Renal Ischemia ◽

Renal Ischemia Reperfusion Injury ◽

Nitric Oxide Pathway

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The Role of Vasodilator Receptors of Renin–angiotensin System on Nitric Oxide Formation and Kidney Circulation after Angiotensin II Infusion in Renal Ischemia/Reperfusion Rats

Advanced Biomedical Research ◽

10.4103/2277-9175.225596 ◽

2018 ◽

Vol 7 (1) ◽

pp. 25 ◽

Cited By ~ 1

Author(s):

Maryam Maleki ◽

Jalal Hasanshahi ◽

Fatemeh Moslemi

Keyword(s):

Nitric Oxide ◽

Angiotensin Ii ◽

Ischemia Reperfusion ◽

Renin Angiotensin System ◽

Renal Ischemia ◽

Oxide Formation ◽

Angiotensin System ◽

Renin Angiotensin ◽

Nitric Oxide Formation

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Faculty Opinions recommendation of Inhibition of cystathionine-beta-synthase activity during renal ischemia-reperfusion: role of pH and nitric oxide.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1120215.576372 ◽

2008 ◽

Author(s):

Roland Blantz

Keyword(s):

Nitric Oxide ◽

Ischemia Reperfusion ◽

Renal Ischemia ◽

Cystathionine Beta Synthase

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Stenosis-dependent role of nitric oxide and prostaglandins in chronic renal ischemia

AJP Renal Physiology ◽

10.1152/ajprenal.00012.2001 ◽

2002 ◽

Vol 282 (5) ◽

pp. F859-F865 ◽

Cited By ~ 13

Author(s):

Hirobumi Tokuyama ◽

Koichi Hayashi ◽

Hiroto Matsuda ◽

Eiji Kubota ◽

Masanori Honda ◽

...

Keyword(s):

Nitric Oxide ◽

Renal Artery ◽

Renal Artery Stenosis ◽

Renal Plasma Flow ◽

Renal Hemodynamics ◽

Renal Ischemia ◽

Artery Stenosis ◽

Left Renal Artery ◽

Severe Stenosis

The role of nitric oxide (NO) and prostaglandins (PG) in modifying renal hemodynamics was examined in clipped and nonclipped kidneys of unilateral renal artery stenosis. Chronic unilateral renal ischemia was established by 4-wk-clipping the left renal artery of canine kidneys, and renal interstitial nitrate+nitrite and PGE2 contents were evaluated by the microdialysis technique. Unilateral renal artery stenosis caused 45 ± 1 and 73 ± 1% decrements in renal plasma flow (RPF) in moderately and severely clipped kidneys and 21 ± 3% decrements in nonclipped kidneys with severe stenosis. Renal nitrate+nitrite decreased in moderately (−31 ± 1%) and severely clipped kidneys (−63 ± 4%). N ω-nitro-l-arginine methyl ester reduced RPF (−56 ± 3%) and glomerular filtration rate (GFR; −54 ± 3%) in moderately clipped kidneys, whereas this inhibitory effect was abolished in severely clipped kidneys. In contrast, renal PGE2 contents increased modestly in moderate clipping and were markedly elevated in severely clipped kidneys (from 111 ± 7 to 377 ± 22 pg/ml); sulpyrine impaired renal hemodynamics only in severely clipped kidneys. In contralateral nonclipped kidneys, although renal PGE2 was not increased, sulpyrine reduced RPF (−32 ± 1%) and GFR (−33 ± 3%) in severe stenosis. Collectively, NO plays a substantial role in maintaining renal hemodynamics both under basal condition and in moderate renal artery stenosis, whereas the contributory role shifts from NO to PG as renal artery stenosis progresses. Furthermore, because intrarenal angiotensin II is reported to increase in nonclipped kidneys, unilateral severe ischemia may render the nonclipped kidney susceptible to PG inhibition.

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