AI Article Synopsis
- Recent research indicates that diabetes can lead to pulmonary hypertension by causing problems in the blood vessels of the lungs.
- In a study using diabetic rats, researchers found that these animals had a reduced ability for their pulmonary arteries to relax when exposed to acetylcholine, suggesting endothelial dysfunction.
- The dysfunction was linked to increased production of superoxide due to NADPH oxidase activity, and this effect could be reversed with specific inhibitors, highlighting potential therapeutic targets for managing diabetes-related vascular issues.
Article Abstract
Recent data suggest that diabetes is a risk factor for pulmonary hypertension. The aim of the present study was to analyze whether diabetes induces endothelial dysfunction in pulmonary arteries and the mechanisms involved. Male Sprague-Dawley rats were randomly divided into a control (saline) and a diabetic group (70 mg/kg(-1) streptozotocin). After 6 wk, intrapulmonary arteries were mounted for isometric tension recording, and endothelial function was tested by the relaxant response to acetylcholine. Protein expression and localization were measured by Western blot and immunohistochemistry and superoxide production by dihydroethidium staining. Pulmonary arteries from diabetic rats showed impaired relaxant response to acetylcholine and reduced vasoconstrictor response to the nitric oxide (NO) synthase inhibitor L-NAME, whereas the response to nitroprusside and the expression of endothelial NO synthase remained unchanged. Endothelial dysfunction was reversed by addition of superoxide dismutase or the NADPH oxidase inhibitor apocynin. An increase in superoxide production and increased expression of the NADPH oxidase regulatory subunit p47(phox) were also found in pulmonary arteries from diabetic rats. In conclusion, the pulmonary circulation is a target for diabetes-induced endothelial dysfunction via enhanced NADPH oxidase-derived superoxide production.
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| http://dx.doi.org/10.1152/ajplung.90354.2008 | DOI Listing |
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