Abstract
Recent data suggest that diabetes is a risk factor for pulmonary hypertension. Several lines of evidence suggest that serotonin is a pathogenetic factor in pulmonary hypertension. We have also recently found pulmonary endothelial dysfunction in diabetic rats. The aim of the present study was to analyze whether diabetes induces changes in the response to serotonin in rat pulmonary arteries and the mechanisms involved. Male Sprague‐Dawley rats were randomly divided into a control (saline) and a diabetic group (70 mg/kg streptozotocin). After 6 weeks, the responses to serotonin were enhanced in pulmonary arteries from diabetic rats. This hyperresponsiveness was endothelium‐independent and unaffected by inhibition of NO synthase but prevented by the cyclooxygenase (COX) inhibitor indomethacin, by superoxide dismutase and by the NADPH oxidase inhibitor apocynin. Lungs from diabetic animals showed an increased expression of COX‐2 as measured by Western blot analysis. In conclusion, as has been described in animal models of pulmonary hypertension, pulmonary arteries from diabetic animals show hyperresposiveness to serotonin. This effect appears to be related to COX‐2 derived metabolites and NADPH oxidase‐induced superoxide production. Supported by Comisi ón Interministerial de Ciencia y Tecnología (CICYT SAF2008‐03948).
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