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Nitric oxide-dependent pulmonary vasodilation in polycythemic rats.
B R Walker1, T C Resta, L D Nelin
1Vascular Physiology Group, Departments of Cell Biology and Physiology and Pediatrics, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131, USA. bwalker@salud.unm.edu
American Journal of Physiology. Heart and Circulatory Physiology
|October 25, 2000
Summary
Increased red blood cell count (polycythemia) does not alter pulmonary endothelial nitric oxide synthase (eNOS) expression or nitric oxide (NO) production, even with elevated vascular shear stress. This suggests polycythemia
Area of Science:
- Physiology
- Cardiovascular Research
- Pulmonary Hypertension
Background:
- Polycythemia elevates vascular shear stress, potentially increasing nitric oxide (NO) production via endothelial nitric oxide synthase (eNOS).
- Both polycythemia and elevated eNOS are linked to pulmonary hypertension, suggesting a potential relationship independent of hypoxia.
Purpose of the Study:
- To investigate if increased hematocrit (polycythemia) upregulates pulmonary eNOS and enhances NO production without hypoxia.
- To test the hypothesis that elevated vascular shear stress in polycythemia alters pulmonary eNOS expression.
Main Methods:
- Rats received erythropoietin (rEpo) to induce polycythemia or a vehicle control.
- Isolated lungs were used to assess vasodilatory responses to ionomycin and vasoconstrictor responses to U-46619.
- Perfusate nitrite/nitrate levels and lung eNOS expression via Western blot were measured.
Main Results:
- Erythropoietin treatment significantly increased hematocrit but did not alter mean pulmonary artery pressure.
- Vasodilatory responses to ionomycin were similar between groups.
- Vasoconstriction to U-46619 was reduced in the rEpo group, but perfusate nitrite/nitrate and lung eNOS levels were unchanged.
Conclusions:
- Increased hematocrit and associated vascular shear stress do not lead to altered pulmonary eNOS expression.
- The study did not find evidence supporting a direct link between polycythemia-induced shear stress and increased pulmonary NO production via eNOS upregulation.