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Bicarbonate-dependent superoxide release and pulmonary artery tone
Eva Nozik-Grayck1, Yuh-Chin T Huang, Martha Sue Carraway
1Department of Pediatrics, Duke University Medical Center, Durham, NC 27710,USA. grayc001@mc.duke.edu
Summary
Extracellular superoxide (O2-*) regulates pulmonary vascular tone by interacting with the bicarbonate-chloride exchanger (AE2). This mechanism is crucial for understanding pulmonary vasoconstriction and hypoxia-induced changes.
Area of Science:
- Cardiovascular Physiology
- Pulmonary Circulation
- Cellular Biology
Background:
- Pulmonary vasoconstriction involves nitric oxide (NO) inactivation by extracellular superoxide (O2-*).
- Mechanisms of O2-* release from pulmonary vascular cells are not fully understood.
- The bicarbonate-chloride anion exchanger AE2 is expressed in the lung.
Purpose of the Study:
- To determine if O2-* release, influencing pulmonary vascular tone, depends on extracellular bicarbonate (HCO3-).
- To investigate the role of AE2 in O2-* release and pulmonary vascular regulation.
Main Methods:
- Assessed vascular reactivity and O2-* release in rat pulmonary artery (PA) rings.
- Compared normal rats with rats exposed to 3 days of hypoxia.
- Utilized bicarbonate (HCO3-) elimination, AE2 inhibitor (SITS), and NO synthase inhibitor (NG-nitro-L-arginine methyl ester).
Main Results:
- Lack of extracellular HCO3- attenuated O2-* release, opposed hypoxic vasoconstriction, and enhanced vasodilation in normal PA rings.
- Hypoxia increased PA AE2 expression and O2-* release, independent of NO synthase.
- AE2 inhibition reduced O2-* release in normoxia.
Conclusions:
- Extracellular bicarbonate influences O2-* release and pulmonary vascular tone.
- AE2 plays a role in mediating O2-* release in the pulmonary circulation.
- O2-* produced by endothelial NOS in normoxia and other sources in hypoxia regulate pulmonary vascular tone via AE2.