TY - JOUR
T1 - Nitric oxide in the vasculature
T2 - Where does it come from and where does it go? A quantitative perspective
AU - Chen, Kejing
AU - Pittman, Roland N.
AU - Popel, Aleksander S.
N1 - Funding Information:
The authors would like to acknowledge the National Natural Science Foundation of China (No. 51206117) and Doctoral Fund of Ministry of Education of China (No. 20120032120004) for grants and supports.
PY - 2008/7/1
Y1 - 2008/7/1
N2 - Nitric oxide (NO) affects two key aspects of O2 supply and demand: It regulates vascular tone and blood flow by activating soluble guanylate cyclase (sGC) in the vascular smooth muscle, and it controls mitochondrial O2 consumption by inhibiting cytochrome c oxidase. However, significant gaps exist in our quantitative understanding of the regulation of NO production in the vascular region. Large apparent discrepancies exist among the published reports that have analyzed the various pathways in terms of the perivascular NO concentration, the efficacy of NO in causing vasodilation (EC50), its efficacy in tissue respiration (IC 50), and the paracrine and endocrine NO release. In this study, we review the NO literature, analyzing NO levels on various scales, identifying and analyzing the discrepancies in the reported data, and proposing hypotheses that can potentially reconcile these discrepancies. Resolving these issues is highly relevant to improving our understanding of vascular biology and to developing pharmaceutical agents that target NO pathways, such as vasodilating drugs.
AB - Nitric oxide (NO) affects two key aspects of O2 supply and demand: It regulates vascular tone and blood flow by activating soluble guanylate cyclase (sGC) in the vascular smooth muscle, and it controls mitochondrial O2 consumption by inhibiting cytochrome c oxidase. However, significant gaps exist in our quantitative understanding of the regulation of NO production in the vascular region. Large apparent discrepancies exist among the published reports that have analyzed the various pathways in terms of the perivascular NO concentration, the efficacy of NO in causing vasodilation (EC50), its efficacy in tissue respiration (IC 50), and the paracrine and endocrine NO release. In this study, we review the NO literature, analyzing NO levels on various scales, identifying and analyzing the discrepancies in the reported data, and proposing hypotheses that can potentially reconcile these discrepancies. Resolving these issues is highly relevant to improving our understanding of vascular biology and to developing pharmaceutical agents that target NO pathways, such as vasodilating drugs.
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U2 - 10.1089/ars.2007.1959
DO - 10.1089/ars.2007.1959
M3 - Review article
C2 - 18331202
AN - SCOPUS:42949114897
VL - 10
SP - 1185
EP - 1198
JO - Antioxidants and Redox Signaling
JF - Antioxidants and Redox Signaling
SN - 1523-0864
IS - 7
ER -