Oxygen indirectly regulates nitric oxide availability

Philip E. James; J. Joan Parton; Simon K. Jackson; Michael P. Frenneaux

Oxygen indirectly regulates nitric oxide availability

Philip E. James^*, J. Joan Parton, Simon K. Jackson, Michael P. Frenneaux

^*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceeding › Chapter › peer-review

2 Citations (Scopus)

Abstract

Oxygen is a critical substrate for both nitric oxide (NO) and superoxide (02-) biosynthesis. Previous studies have established that constitutive calcium-dependent NO synthase (NOS) and 02 producing NADPH-oxidase are affected at the level of gene expression and at a functional level. For example, hypoxia increases expression of the genes encoding both macrophage and endothelial NOS isoforms, and low oxygen tension attenuates NOS activity and NO-dependent vascular relaxation. Both NOS and NADPH-oxidase participate in modulation of vascular tone ° although how oxygen regulates endothelial response is unclear. We have previously demonstrated the dependence of macrophage NADPH-oxidase on the cellular distribution of oxygen, and both superoxide and NO production by endothelial cells.

Original language	English
Title of host publication	Oxygen Transport To Tissue XXIII
Subtitle of host publication	Oxygen Measurements in the 21st Century: Basic Techniques and Clinical Relevance
Pages	139-143
Number of pages	5
Publication status	Published - 2003
Externally published	Yes

Publication series

Name	Advances in Experimental Medicine and Biology
Volume	510
ISSN (Print)	0065-2598

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https://link.springer.com/chapter/10.1007/978-1-4615-0205-0_23

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James, P. E., Parton, J. J., Jackson, S. K., & Frenneaux, M. P. (2003). Oxygen indirectly regulates nitric oxide availability. In Oxygen Transport To Tissue XXIII: Oxygen Measurements in the 21st Century: Basic Techniques and Clinical Relevance (pp. 139-143). (Advances in Experimental Medicine and Biology; Vol. 510). https://link.springer.com/chapter/10.1007/978-1-4615-0205-0_23

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abstract = "Oxygen is a critical substrate for both nitric oxide (NO) and superoxide (02-) biosynthesis. Previous studies have established that constitutive calcium-dependent NO synthase (NOS) and 02 producing NADPH-oxidase are affected at the level of gene expression and at a functional level. For example, hypoxia increases expression of the genes encoding both macrophage and endothelial NOS isoforms, and low oxygen tension attenuates NOS activity and NO-dependent vascular relaxation. Both NOS and NADPH-oxidase participate in modulation of vascular tone ° although how oxygen regulates endothelial response is unclear. We have previously demonstrated the dependence of macrophage NADPH-oxidase on the cellular distribution of oxygen, and both superoxide and NO production by endothelial cells.",

author = "James, {Philip E.} and Parton, {J. Joan} and Jackson, {Simon K.} and Frenneaux, {Michael P.}",

year = "2003",

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Oxygen indirectly regulates nitric oxide availability. / James, Philip E.; Parton, J. Joan; Jackson, Simon K. et al.
Oxygen Transport To Tissue XXIII: Oxygen Measurements in the 21st Century: Basic Techniques and Clinical Relevance. 2003. p. 139-143 (Advances in Experimental Medicine and Biology; Vol. 510).

Research output: Chapter in Book/Report/Conference proceeding › Chapter › peer-review

TY - CHAP

T1 - Oxygen indirectly regulates nitric oxide availability

AU - James, Philip E.

AU - Parton, J. Joan

AU - Jackson, Simon K.

AU - Frenneaux, Michael P.

PY - 2003

Y1 - 2003

N2 - Oxygen is a critical substrate for both nitric oxide (NO) and superoxide (02-) biosynthesis. Previous studies have established that constitutive calcium-dependent NO synthase (NOS) and 02 producing NADPH-oxidase are affected at the level of gene expression and at a functional level. For example, hypoxia increases expression of the genes encoding both macrophage and endothelial NOS isoforms, and low oxygen tension attenuates NOS activity and NO-dependent vascular relaxation. Both NOS and NADPH-oxidase participate in modulation of vascular tone ° although how oxygen regulates endothelial response is unclear. We have previously demonstrated the dependence of macrophage NADPH-oxidase on the cellular distribution of oxygen, and both superoxide and NO production by endothelial cells.

AB - Oxygen is a critical substrate for both nitric oxide (NO) and superoxide (02-) biosynthesis. Previous studies have established that constitutive calcium-dependent NO synthase (NOS) and 02 producing NADPH-oxidase are affected at the level of gene expression and at a functional level. For example, hypoxia increases expression of the genes encoding both macrophage and endothelial NOS isoforms, and low oxygen tension attenuates NOS activity and NO-dependent vascular relaxation. Both NOS and NADPH-oxidase participate in modulation of vascular tone ° although how oxygen regulates endothelial response is unclear. We have previously demonstrated the dependence of macrophage NADPH-oxidase on the cellular distribution of oxygen, and both superoxide and NO production by endothelial cells.

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M3 - Chapter

C2 - 12580418

AN - SCOPUS:0037227932

T3 - Advances in Experimental Medicine and Biology

SP - 139

EP - 143

BT - Oxygen Transport To Tissue XXIII

ER -

Oxygen indirectly regulates nitric oxide availability

Abstract

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