NITRIC OXIDE-DEPENDENT ENDOTHELIAL FUNCTION IS UNAFFECTED BY ALLOPURINOL IN HYPERCHOLESTEROLAEMIC SUBJECTS
1. Hypercholesterolaemia is associated with abnormal endothelium-related vasodilator function, possibly due to increased destruction •NO by superoxide anions (•O2–). Oxypurinol, a xanthine oxidase (XO) inhibitor with anti-oxidant properties and the active metabolite of the commonly used drug allopur...
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| Autor*in: |
O’Driscoll, JG [verfasserIn] Green, DJ [verfasserIn] Rankin, JM [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Melbourne, Australia: Blackwell Science Pty ; 1999 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2001 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Clinical and experimental pharmacology and physiology - Oxford [u.a.] : Wiley-Blackwell, 1974, 26(1999), 10, Seite 0 |
| Übergeordnetes Werk: |
volume:26 ; year:1999 ; number:10 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1046/j.1440-1681.1999.03125.x |
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NLEJ242578454 |
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| 520 | |a 1. Hypercholesterolaemia is associated with abnormal endothelium-related vasodilator function, possibly due to increased destruction •NO by superoxide anions (•O2–). Oxypurinol, a xanthine oxidase (XO) inhibitor with anti-oxidant properties and the active metabolite of the commonly used drug allopurinol, reduces •NO quenching in vitro and has been reported to acutely improve endothelial function in hypercholesterolaemic subjects.2. The purpose of the present study was to determine whether oral allopurinol improves •NO dilator function in hypercholesterolaemic subjects.3. A randomized double-blind, placebo-controlled cross-over design evaluated the effect of allopurinol (300 mg daily for 4 weeks) on forearm blood flow (FBF) responses to intrabrachial infusion of acetylcholine (ACh), sodium nitroprusside (SNP) and NG-monomethyl- L-arginine ( L-NMMA) in nine hypercholesterolaemic subjects.4. Endothelium-dependent vascular responses to ACh and L-NMMA were not significantly altered by allopurinol. The endothelium-independent vasodilator response to SNP was similarly unchanged.5. These results indicate that allopurinol does not influence basal or stimulated activity of the •NO dilator system in hypercholesterolaemic subjects. If intracellular •O2– inactivation •NO is responsible for endothelial dysfunction in hypercholesterolaemia, the source may be other than XO dependent. However, generation of •O2– during the conversion of allopurinol to oxypurinol could offer an alternative, and probably more likely, explanation for the ineffectiveness of allopurinol in vivo. | ||
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10.1046/j.1440-1681.1999.03125.x doi (DE-627)NLEJ242578454 DE-627 ger DE-627 rakwb O’Driscoll, JG verfasserin aut NITRIC OXIDE-DEPENDENT ENDOTHELIAL FUNCTION IS UNAFFECTED BY ALLOPURINOL IN HYPERCHOLESTEROLAEMIC SUBJECTS Melbourne, Australia Blackwell Science Pty 1999 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 1. Hypercholesterolaemia is associated with abnormal endothelium-related vasodilator function, possibly due to increased destruction •NO by superoxide anions (•O2–). Oxypurinol, a xanthine oxidase (XO) inhibitor with anti-oxidant properties and the active metabolite of the commonly used drug allopurinol, reduces •NO quenching in vitro and has been reported to acutely improve endothelial function in hypercholesterolaemic subjects.2. The purpose of the present study was to determine whether oral allopurinol improves •NO dilator function in hypercholesterolaemic subjects.3. A randomized double-blind, placebo-controlled cross-over design evaluated the effect of allopurinol (300 mg daily for 4 weeks) on forearm blood flow (FBF) responses to intrabrachial infusion of acetylcholine (ACh), sodium nitroprusside (SNP) and NG-monomethyl- L-arginine ( L-NMMA) in nine hypercholesterolaemic subjects.4. Endothelium-dependent vascular responses to ACh and L-NMMA were not significantly altered by allopurinol. The endothelium-independent vasodilator response to SNP was similarly unchanged.5. These results indicate that allopurinol does not influence basal or stimulated activity of the •NO dilator system in hypercholesterolaemic subjects. If intracellular •O2– inactivation •NO is responsible for endothelial dysfunction in hypercholesterolaemia, the source may be other than XO dependent. However, generation of •O2– during the conversion of allopurinol to oxypurinol could offer an alternative, and probably more likely, explanation for the ineffectiveness of allopurinol in vivo. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| allopurinol Green, DJ verfasserin aut Rankin, JM verfasserin aut Taylor, RR oth In Clinical and experimental pharmacology and physiology Oxford [u.a.] : Wiley-Blackwell, 1974 26(1999), 10, Seite 0 Online-Ressource (DE-627)NLEJ243927150 (DE-600)2020033-X 1440-1681 nnns volume:26 year:1999 number:10 pages:0 http://dx.doi.org/10.1046/j.1440-1681.1999.03125.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 26 1999 10 0 |
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10.1046/j.1440-1681.1999.03125.x doi (DE-627)NLEJ242578454 DE-627 ger DE-627 rakwb O’Driscoll, JG verfasserin aut NITRIC OXIDE-DEPENDENT ENDOTHELIAL FUNCTION IS UNAFFECTED BY ALLOPURINOL IN HYPERCHOLESTEROLAEMIC SUBJECTS Melbourne, Australia Blackwell Science Pty 1999 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 1. Hypercholesterolaemia is associated with abnormal endothelium-related vasodilator function, possibly due to increased destruction •NO by superoxide anions (•O2–). Oxypurinol, a xanthine oxidase (XO) inhibitor with anti-oxidant properties and the active metabolite of the commonly used drug allopurinol, reduces •NO quenching in vitro and has been reported to acutely improve endothelial function in hypercholesterolaemic subjects.2. The purpose of the present study was to determine whether oral allopurinol improves •NO dilator function in hypercholesterolaemic subjects.3. A randomized double-blind, placebo-controlled cross-over design evaluated the effect of allopurinol (300 mg daily for 4 weeks) on forearm blood flow (FBF) responses to intrabrachial infusion of acetylcholine (ACh), sodium nitroprusside (SNP) and NG-monomethyl- L-arginine ( L-NMMA) in nine hypercholesterolaemic subjects.4. Endothelium-dependent vascular responses to ACh and L-NMMA were not significantly altered by allopurinol. The endothelium-independent vasodilator response to SNP was similarly unchanged.5. These results indicate that allopurinol does not influence basal or stimulated activity of the •NO dilator system in hypercholesterolaemic subjects. If intracellular •O2– inactivation •NO is responsible for endothelial dysfunction in hypercholesterolaemia, the source may be other than XO dependent. However, generation of •O2– during the conversion of allopurinol to oxypurinol could offer an alternative, and probably more likely, explanation for the ineffectiveness of allopurinol in vivo. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| allopurinol Green, DJ verfasserin aut Rankin, JM verfasserin aut Taylor, RR oth In Clinical and experimental pharmacology and physiology Oxford [u.a.] : Wiley-Blackwell, 1974 26(1999), 10, Seite 0 Online-Ressource (DE-627)NLEJ243927150 (DE-600)2020033-X 1440-1681 nnns volume:26 year:1999 number:10 pages:0 http://dx.doi.org/10.1046/j.1440-1681.1999.03125.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 26 1999 10 0 |
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10.1046/j.1440-1681.1999.03125.x doi (DE-627)NLEJ242578454 DE-627 ger DE-627 rakwb O’Driscoll, JG verfasserin aut NITRIC OXIDE-DEPENDENT ENDOTHELIAL FUNCTION IS UNAFFECTED BY ALLOPURINOL IN HYPERCHOLESTEROLAEMIC SUBJECTS Melbourne, Australia Blackwell Science Pty 1999 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 1. Hypercholesterolaemia is associated with abnormal endothelium-related vasodilator function, possibly due to increased destruction •NO by superoxide anions (•O2–). Oxypurinol, a xanthine oxidase (XO) inhibitor with anti-oxidant properties and the active metabolite of the commonly used drug allopurinol, reduces •NO quenching in vitro and has been reported to acutely improve endothelial function in hypercholesterolaemic subjects.2. The purpose of the present study was to determine whether oral allopurinol improves •NO dilator function in hypercholesterolaemic subjects.3. A randomized double-blind, placebo-controlled cross-over design evaluated the effect of allopurinol (300 mg daily for 4 weeks) on forearm blood flow (FBF) responses to intrabrachial infusion of acetylcholine (ACh), sodium nitroprusside (SNP) and NG-monomethyl- L-arginine ( L-NMMA) in nine hypercholesterolaemic subjects.4. Endothelium-dependent vascular responses to ACh and L-NMMA were not significantly altered by allopurinol. The endothelium-independent vasodilator response to SNP was similarly unchanged.5. These results indicate that allopurinol does not influence basal or stimulated activity of the •NO dilator system in hypercholesterolaemic subjects. If intracellular •O2– inactivation •NO is responsible for endothelial dysfunction in hypercholesterolaemia, the source may be other than XO dependent. However, generation of •O2– during the conversion of allopurinol to oxypurinol could offer an alternative, and probably more likely, explanation for the ineffectiveness of allopurinol in vivo. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| allopurinol Green, DJ verfasserin aut Rankin, JM verfasserin aut Taylor, RR oth In Clinical and experimental pharmacology and physiology Oxford [u.a.] : Wiley-Blackwell, 1974 26(1999), 10, Seite 0 Online-Ressource (DE-627)NLEJ243927150 (DE-600)2020033-X 1440-1681 nnns volume:26 year:1999 number:10 pages:0 http://dx.doi.org/10.1046/j.1440-1681.1999.03125.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 26 1999 10 0 |
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10.1046/j.1440-1681.1999.03125.x doi (DE-627)NLEJ242578454 DE-627 ger DE-627 rakwb O’Driscoll, JG verfasserin aut NITRIC OXIDE-DEPENDENT ENDOTHELIAL FUNCTION IS UNAFFECTED BY ALLOPURINOL IN HYPERCHOLESTEROLAEMIC SUBJECTS Melbourne, Australia Blackwell Science Pty 1999 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 1. Hypercholesterolaemia is associated with abnormal endothelium-related vasodilator function, possibly due to increased destruction •NO by superoxide anions (•O2–). Oxypurinol, a xanthine oxidase (XO) inhibitor with anti-oxidant properties and the active metabolite of the commonly used drug allopurinol, reduces •NO quenching in vitro and has been reported to acutely improve endothelial function in hypercholesterolaemic subjects.2. The purpose of the present study was to determine whether oral allopurinol improves •NO dilator function in hypercholesterolaemic subjects.3. A randomized double-blind, placebo-controlled cross-over design evaluated the effect of allopurinol (300 mg daily for 4 weeks) on forearm blood flow (FBF) responses to intrabrachial infusion of acetylcholine (ACh), sodium nitroprusside (SNP) and NG-monomethyl- L-arginine ( L-NMMA) in nine hypercholesterolaemic subjects.4. Endothelium-dependent vascular responses to ACh and L-NMMA were not significantly altered by allopurinol. The endothelium-independent vasodilator response to SNP was similarly unchanged.5. These results indicate that allopurinol does not influence basal or stimulated activity of the •NO dilator system in hypercholesterolaemic subjects. If intracellular •O2– inactivation •NO is responsible for endothelial dysfunction in hypercholesterolaemia, the source may be other than XO dependent. However, generation of •O2– during the conversion of allopurinol to oxypurinol could offer an alternative, and probably more likely, explanation for the ineffectiveness of allopurinol in vivo. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| allopurinol Green, DJ verfasserin aut Rankin, JM verfasserin aut Taylor, RR oth In Clinical and experimental pharmacology and physiology Oxford [u.a.] : Wiley-Blackwell, 1974 26(1999), 10, Seite 0 Online-Ressource (DE-627)NLEJ243927150 (DE-600)2020033-X 1440-1681 nnns volume:26 year:1999 number:10 pages:0 http://dx.doi.org/10.1046/j.1440-1681.1999.03125.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 26 1999 10 0 |
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O’Driscoll, JG Green, DJ Rankin, JM |
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O’Driscoll, JG |
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nitric oxide-dependent endothelial function is unaffected by allopurinol in hypercholesterolaemic subjects |
| title_auth |
NITRIC OXIDE-DEPENDENT ENDOTHELIAL FUNCTION IS UNAFFECTED BY ALLOPURINOL IN HYPERCHOLESTEROLAEMIC SUBJECTS |
| abstract |
1. Hypercholesterolaemia is associated with abnormal endothelium-related vasodilator function, possibly due to increased destruction •NO by superoxide anions (•O2–). Oxypurinol, a xanthine oxidase (XO) inhibitor with anti-oxidant properties and the active metabolite of the commonly used drug allopurinol, reduces •NO quenching in vitro and has been reported to acutely improve endothelial function in hypercholesterolaemic subjects.2. The purpose of the present study was to determine whether oral allopurinol improves •NO dilator function in hypercholesterolaemic subjects.3. A randomized double-blind, placebo-controlled cross-over design evaluated the effect of allopurinol (300 mg daily for 4 weeks) on forearm blood flow (FBF) responses to intrabrachial infusion of acetylcholine (ACh), sodium nitroprusside (SNP) and NG-monomethyl- L-arginine ( L-NMMA) in nine hypercholesterolaemic subjects.4. Endothelium-dependent vascular responses to ACh and L-NMMA were not significantly altered by allopurinol. The endothelium-independent vasodilator response to SNP was similarly unchanged.5. These results indicate that allopurinol does not influence basal or stimulated activity of the •NO dilator system in hypercholesterolaemic subjects. If intracellular •O2– inactivation •NO is responsible for endothelial dysfunction in hypercholesterolaemia, the source may be other than XO dependent. However, generation of •O2– during the conversion of allopurinol to oxypurinol could offer an alternative, and probably more likely, explanation for the ineffectiveness of allopurinol in vivo. |
| abstractGer |
1. Hypercholesterolaemia is associated with abnormal endothelium-related vasodilator function, possibly due to increased destruction •NO by superoxide anions (•O2–). Oxypurinol, a xanthine oxidase (XO) inhibitor with anti-oxidant properties and the active metabolite of the commonly used drug allopurinol, reduces •NO quenching in vitro and has been reported to acutely improve endothelial function in hypercholesterolaemic subjects.2. The purpose of the present study was to determine whether oral allopurinol improves •NO dilator function in hypercholesterolaemic subjects.3. A randomized double-blind, placebo-controlled cross-over design evaluated the effect of allopurinol (300 mg daily for 4 weeks) on forearm blood flow (FBF) responses to intrabrachial infusion of acetylcholine (ACh), sodium nitroprusside (SNP) and NG-monomethyl- L-arginine ( L-NMMA) in nine hypercholesterolaemic subjects.4. Endothelium-dependent vascular responses to ACh and L-NMMA were not significantly altered by allopurinol. The endothelium-independent vasodilator response to SNP was similarly unchanged.5. These results indicate that allopurinol does not influence basal or stimulated activity of the •NO dilator system in hypercholesterolaemic subjects. If intracellular •O2– inactivation •NO is responsible for endothelial dysfunction in hypercholesterolaemia, the source may be other than XO dependent. However, generation of •O2– during the conversion of allopurinol to oxypurinol could offer an alternative, and probably more likely, explanation for the ineffectiveness of allopurinol in vivo. |
| abstract_unstemmed |
1. Hypercholesterolaemia is associated with abnormal endothelium-related vasodilator function, possibly due to increased destruction •NO by superoxide anions (•O2–). Oxypurinol, a xanthine oxidase (XO) inhibitor with anti-oxidant properties and the active metabolite of the commonly used drug allopurinol, reduces •NO quenching in vitro and has been reported to acutely improve endothelial function in hypercholesterolaemic subjects.2. The purpose of the present study was to determine whether oral allopurinol improves •NO dilator function in hypercholesterolaemic subjects.3. A randomized double-blind, placebo-controlled cross-over design evaluated the effect of allopurinol (300 mg daily for 4 weeks) on forearm blood flow (FBF) responses to intrabrachial infusion of acetylcholine (ACh), sodium nitroprusside (SNP) and NG-monomethyl- L-arginine ( L-NMMA) in nine hypercholesterolaemic subjects.4. Endothelium-dependent vascular responses to ACh and L-NMMA were not significantly altered by allopurinol. The endothelium-independent vasodilator response to SNP was similarly unchanged.5. These results indicate that allopurinol does not influence basal or stimulated activity of the •NO dilator system in hypercholesterolaemic subjects. If intracellular •O2– inactivation •NO is responsible for endothelial dysfunction in hypercholesterolaemia, the source may be other than XO dependent. However, generation of •O2– during the conversion of allopurinol to oxypurinol could offer an alternative, and probably more likely, explanation for the ineffectiveness of allopurinol in vivo. |
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NITRIC OXIDE-DEPENDENT ENDOTHELIAL FUNCTION IS UNAFFECTED BY ALLOPURINOL IN HYPERCHOLESTEROLAEMIC SUBJECTS |
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