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Title:
The effect of insufficiency of tetrahydrobiopterin on endothelial function and vasoactivity | General Thoracic and Cardiovascular Surgery
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Objective: It has recently been defined that levels of tetrahydrobiopterin, a cofactor of nitric oxide synthase, decreases under some disease conditions including atherosclerosis, hypercholesterolemia, diabetes, and ischemia-reperfusion. The present study was designed to investigate whether or not a deficiency in tetrahydrobiopterin affected vasoactivation in vivo and in vitro.Subjects and Methods: Male Sprague-Dawley rats were divided into two groups, and given either 2, 4-diamino-6-hydroxypyrimidine (DAHP), a selective inhibitor of tetrahydrobiopterin production, or a vehicle (10% polyethylene glycol 400 in 5% glucose, 20 ml/kg), intraperitoneally at 24 hr prior to examination. Responses to several vasodilating agents were examined in both pretreatment groups in vivo and in vitro. Furthermore, the isolated heart was perfused with a 37ยฐC Krebs-Henseleit solution for 30 min. The effects of insufficient tetrahydrobiopterin on the left ventricular function were examined. Moreover, nitrite plus nitrate (NOx) in the coronary effluent was examined in both groups.Results: Depressor and vasodilatation responses to an endothelium-dependent vasodilator were significantly attenuated in the DAHP Group in comparison with those in the vehicle Control Group, while the endothelium-independent vasodilator caused equivalent depressor and vasodilatation responses between the two groups. The NOx levels in the coronary effluent were lower in the DAHP Group than in the Control Group (p<0.05). The cardiovascular parameters were also lower in the DAHP Group than in the Control Group. Conclusions: We concluded from these findings that a deficiency in tetrahydrobiopterin aggravated endothelial dysfunction and the left ventricular dysfunction. These findings were consistent with the hypothesis that decreased levels of tetrahydrobiopterin may cause cardiac and vascular dysfunction.
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article, tetrahydrobiopterin, google, scholar, pubmed, cas, endothelial, nitric, function, oxide, dysfunction, content, effect, synthase, group, privacy, cookies, journal, cardiovascular, yamashiro, access, publish, search, miyagi, disease, dahp, vasodilator, injury, data, information, log, research, surgery, kuniyoshi, arakaki, levels, cofactor, ischemiareperfusion, vivo, groups, responses, examined, coronary, endotheliumdependent, control, vascular, discover, biochem, res, cosentino,
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month download article/chapter nitric oxide synthase male sprague-dawley rats endothelium-derived relaxing factor related subjects ischemia-reperfusion injury nitric oxide tetrahidrobiopterin synthasis reduces full article pdf privacy choices/manage cookies vascular endothelial function left ventricular dysfunction endothelium-dependent vasodilator aortic endothelial cells check access instant access spontaneously hypertensive rats guinea pig hearts conditions privacy policy european economic area krebs-henseleit solution dexamethasone suppression test functioning adrenal incidentaloma reactive hyperemia response experimental endotoxic shock left ventricular function tetrahydrobiopterin affected vasoactivation tetrahydrobiopterin-dependent formation ischemia-reperfusion article yamashiro vascular dysfunction accepting optional cookies coronary artery disease reperfusion injury lรผscher tf endothelial dysfunction cardiovascular surgery aims main content log tetrahydrobiopterin-dependent inhibition article log journal finder publish article cite vascular disease endothelial function vehicle control group critical cofactor subjects tetrahydrobiopterin production privacy policy personal data
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- Tetrahydrobiopterin: A critical cofactor for eNOS and a strategy in the treatment of endothelial dysfunction?
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headline:The effect of insufficiency of tetrahydrobiopterin on endothelial function and vasoactivity
description:Objective: It has recently been defined that levels of tetrahydrobiopterin, a cofactor of nitric oxide synthase, decreases under some disease conditions including atherosclerosis, hypercholesterolemia, diabetes, and ischemia-reperfusion. The present study was designed to investigate whether or not a deficiency in tetrahydrobiopterin affected vasoactivation in vivo and in vitro.Subjects and Methods: Male Sprague-Dawley rats were divided into two groups, and given either 2, 4-diamino-6-hydroxypyrimidine (DAHP), a selective inhibitor of tetrahydrobiopterin production, or a vehicle (10% polyethylene glycol 400 in 5% glucose, 20 ml/kg), intraperitoneally at 24 hr prior to examination. Responses to several vasodilating agents were examined in both pretreatment groups in vivo and in vitro. Furthermore, the isolated heart was perfused with a 37ยฐC Krebs-Henseleit solution for 30 min. The effects of insufficient tetrahydrobiopterin on the left ventricular function were examined. Moreover, nitrite plus nitrate (NOx) in the coronary effluent was examined in both groups.Results: Depressor and vasodilatation responses to an endothelium-dependent vasodilator were significantly attenuated in the DAHP Group in comparison with those in the vehicle Control Group, while the endothelium-independent vasodilator caused equivalent depressor and vasodilatation responses between the two groups. The NOx levels in the coronary effluent were lower in the DAHP Group than in the Control Group (p<0.05). The cardiovascular parameters were also lower in the DAHP Group than in the Control Group. Conclusions: We concluded from these findings that a deficiency in tetrahydrobiopterin aggravated endothelial dysfunction and the left ventricular dysfunction. These findings were consistent with the hypothesis that decreased levels of tetrahydrobiopterin may cause cardiac and vascular dysfunction.
datePublished:
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tetrahydrobiopterin
nitric oxide synthase
nitric oxide
endothelial dysfunction
Thoracic Surgery
Cardiac Surgery
Cardiology
Surgical Oncology
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headline:The effect of insufficiency of tetrahydrobiopterin on endothelial function and vasoactivity
description:Objective: It has recently been defined that levels of tetrahydrobiopterin, a cofactor of nitric oxide synthase, decreases under some disease conditions including atherosclerosis, hypercholesterolemia, diabetes, and ischemia-reperfusion. The present study was designed to investigate whether or not a deficiency in tetrahydrobiopterin affected vasoactivation in vivo and in vitro.Subjects and Methods: Male Sprague-Dawley rats were divided into two groups, and given either 2, 4-diamino-6-hydroxypyrimidine (DAHP), a selective inhibitor of tetrahydrobiopterin production, or a vehicle (10% polyethylene glycol 400 in 5% glucose, 20 ml/kg), intraperitoneally at 24 hr prior to examination. Responses to several vasodilating agents were examined in both pretreatment groups in vivo and in vitro. Furthermore, the isolated heart was perfused with a 37ยฐC Krebs-Henseleit solution for 30 min. The effects of insufficient tetrahydrobiopterin on the left ventricular function were examined. Moreover, nitrite plus nitrate (NOx) in the coronary effluent was examined in both groups.Results: Depressor and vasodilatation responses to an endothelium-dependent vasodilator were significantly attenuated in the DAHP Group in comparison with those in the vehicle Control Group, while the endothelium-independent vasodilator caused equivalent depressor and vasodilatation responses between the two groups. The NOx levels in the coronary effluent were lower in the DAHP Group than in the Control Group (p<0.05). The cardiovascular parameters were also lower in the DAHP Group than in the Control Group. Conclusions: We concluded from these findings that a deficiency in tetrahydrobiopterin aggravated endothelial dysfunction and the left ventricular dysfunction. These findings were consistent with the hypothesis that decreased levels of tetrahydrobiopterin may cause cardiac and vascular dysfunction.
datePublished:
dateModified:
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pageEnd:477
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tetrahydrobiopterin
nitric oxide synthase
nitric oxide
endothelial dysfunction
Thoracic Surgery
Cardiac Surgery
Cardiology
Surgical Oncology
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