期刊
ANTIOXIDANTS & REDOX SIGNALING
卷 10, 期 6, 页码 1137-1152出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2007.1995
关键词
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资金
- NHLBI NIH HHS [HL66331, HL31069, R01 HL066331-07, R01 HL085352-01A2, R01 HL031069, R01 HL031069-23, P01 HL043023, R01 HL132574, P01 HL043023-170002, R01 HL085352, R01 HL066331, HL085352, P01 HL043023-17] Funding Source: Medline
- PHS HHS [H43023] Funding Source: Medline
It has been well known for > 100 years that systemic blood vessels dilate in response to decreases in oxygen tension (hypoxia; low Po-2), and this response appears to be critical to supply blood to the stressed organ. Conversely, pulmonary vessels constrict to a decrease in alveolar Po-2 to maintain a balance in the ventilation-toperfusion ratio. Currently, although little question exists that the Po-2 affects vascular reactivity and vascular smooth muscle cells (VSMCs) act as oxygen sensors, the molecular mechanisms involved in modulating the vascular reactivity are still not clearly understood. Many laboratories, including ours, have suggested that the intracellular calcium concentration ([Ca2+](i)), which regulates vasomotor function, is controlled by free radicals and redox signaling, including NAD( P) H and glutathione (GSH) redox. In this review article, therefore, we discuss the implications of redox and oxidant alterations seen in pulmonary and systemic hypertension, and how key targets that control [Ca2+](i), such as ion channels, Ca2+ release from internal stores and uptake by the sarcoplasmic reticulum, and the Ca2+ sensitivity to the myofilaments, are regulated by changes in intracellular redox and oxidants associated with vascular Po-2 sensing in physiologic or pathophysiologic conditions.
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