scholarly journals Preventive effect of gomisin J from Schisandra chinensis on angiotensin II-induced hypertension via an increased nitric oxide bioavailability

2014 ◽  
Vol 38 (3) ◽  
pp. 169-177 ◽  
Author(s):  
Byeong Hyeok Ye ◽  
Seung Jin Lee ◽  
Young Whan Choi ◽  
So Youn Park ◽  
Chi Dae Kim
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Schisandra Chinensis ◽  
Preventive Effect ◽  
Induced Hypertension ◽  
Nitric Oxide Bioavailability

scholarly journals Increased Nitric Oxide Bioavailability in Adult GRK2 Hemizygous Mice Protects Against Angiotensin II–Induced Hypertension

Hypertension ◽  
2014 ◽  
Vol 63 (2) ◽  
pp. 369-375 ◽  
Author(s):  
María S. Avendaño ◽  
Elisa Lucas ◽  
María Jurado-Pueyo ◽  
Sonia Martínez-Revelles ◽  
Rocío Vila-Bedmar ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Induced Hypertension ◽  
Nitric Oxide Bioavailability

scholarly journals Effects of metoprolol on oxidant stress parameters and nitric oxide bioavailability in angiotensin II induced hypertension

2003 ◽  
Vol 41 (6) ◽  
pp. 295
Author(s):  
Ulrich Hink ◽  
Eberhard Schulz ◽  
Hanke Mollnau ◽  
Alexandra von Sandersleben ◽  
Michael August ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Oxidant Stress ◽  
Induced Hypertension ◽  
Nitric Oxide Bioavailability ◽  
Stress Parameters

scholarly journals Endothelium-specific sepiapterin reductase deficiency in DOCA-salt hypertension

2012 ◽  
Vol 302 (11) ◽  
pp. H2243-H2249 ◽  
Author(s):  
Ji Youn Youn ◽  
Ting Wang ◽  
John Blair ◽  
Karine M. Laude ◽  
Jeong-Ho Oak ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Oxidase Inhibitor ◽  
Aortic Endothelial Cells ◽  
Sepiapterin Reductase ◽  
Enos Uncoupling ◽  
Induced Hypertension ◽  
Salt Hypertension ◽  
Endothelial Nitric Oxide ◽  
Aortic Endothelial

The endothelial nitric oxide synthase (eNOS) requires tetrahydrobiopterin (H4B) as a cofactor and, in its absence, produces superoxide (O2·−) rather than nitric oxide (NO·), a condition referred to as eNOS uncoupling. DOCA-salt-induced hypertension is associated with H4B oxidation and uncoupling of eNOS. The present study investigated whether administration of sepiapterin or H4B recouples eNOS in DOCA-salt hypertension. Bioavailable NO· detected by electron spin resonance was markedly reduced in aortas of DOCA-salt hypertensive mice. Preincubation with sepiapterin (10 μmol/l for 30 min) failed to improve NO· bioavailability in hypertensive aortas while it augmented NO· production from control vessels, implicating a hypertension-associated deficiency in sepiapterin reductase (SPR), the rate-limiting enzyme for sepiapterin conversion to H4B. Indeed, a decreased SPR expression was observed in aortic endothelial cells, but not in endothelium-denuded aortic remains, implicating an endothelium-specific SPR deficiency. Administration of hypertensive aortas with H4B (10 μmol/l, 30 min) partially restored vascular NO· production. Combined administration of H4B and the NADPH oxidase inhibitor apocynin (100 μmol/l, 30 min) fully restored NO· bioavailability while reducing O2·− production. In angiotensin II-induced hypertension, however, aortic endothelial SPR expression was not affected. In summary, administration of sepiapterin is not effective in recoupling eNOS in DOCA-salt hypertension, due to an endothelium-specific loss in SPR, whereas coadministration of H4B and apocynin is highly efficient in recoupling eNOS. This is consistent with our previous observations that in angiotensin II hypertension, endothelial deficiency in dihydrofolate reductase is alternatively responsible for uncoupling of eNOS. Taken together, these data indicate that strategies specifically targeting at different H4B metabolic enzymes might be necessary in restoring eNOS function in different types of hypertension.

Role of nitric oxide resistance in erythropoietin-induced hypertension in rats with chronic renal failure

1996 ◽  
Vol 271 (1) ◽  
pp. E113-E122 ◽  
Author(s):  
N. D. Vaziri ◽  
X. J. Zhou ◽  
F. Naqvi ◽  
J. Smith ◽  
F. Oveisi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Magnesium Concentration ◽  
Induced Hypertension ◽  
Group A

We studied the mechanism of erythropoietin (EPO)-induced hypertension (HTN) in rats with chronic renal failure (CRF). After partial nephrectomy, rats were randomized into four groups. Group A received EPO, 150 U/kg, two times weekly for 6 wk to prevent anemia; group B received placebo injections and became anemic; group C received EPO but was kept anemic by dietary iron deficiency; and group D received placebo and regular transfusions to match hematocrit (Hct) in group A. Blood pressure (BP), Hct, platelet cytosolic calcium ([Ca2+]i) and magnesium concentration, and pressor and vasodilatory responses were determined. By design, Hct in groups A and D were comparable and significantly greater (P < 0.01) than in groups B and C. Despite divergent Hct values, the EPO-treated groups A and C showed a significant rise in BP compared with the placebo-treated groups B and D. HTN occurred whether EPO therapy was begun immediately or 4 wk after nephrectomy. EPO therapy augmented the elevation of basal [Ca2+]i and restored the defective thrombin-mediated rise of platelet [Ca2+]i in CRF animals. EPO therapy did not alter caudal artery contraction in response to either 68 mM K(+)-induced depolarization, angiotensin II or alpha 1-agonist, methoxamine in vitro, or the pressor response to angiotensin II in vivo. However, EPO therapy impaired the hypotensive response to nitric oxide (NO) donors, sodium nitroprusside and S-nitroso-N-acetyl-D,L-penicillamine, and reversed the CRF-induced upregulation of guanosine 3',5'-cyclic monophosphate production by thoracic aorta in vitro. Thus EPO-induced HTN in CRF rats is Hct independent and is associated with and perhaps causally related to increased basal and stimulated [Ca2+]i and impaired vasodilatory response to NO.

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