AIM: To investigate the expression of B-type natriuretic peptide-45 (BNP-45) gene which was induced by systemic chronic hypoxia, and whether these changes would be different from BNP-45 protein in the plasma and its mRNA in the ventricular myocardial. This study also aimed to test the hypothesis that systemic chronic hypoxia may cause heart failure. METHODS: Although clinical use of BNP as a biomarker in heart failure is increasing, the specificity of BNP for heart failure is not robust, suggesting that other mechanisms beyond simple ventricular stretch stimulate BNP release. Plasma BNP levels were markedly increased in patients with coronary artery disease but without concomitant left ventricular dysfunction. Thus, elevated BNP levels do not necessarily reflect heart failure but may also result from cardiac ischemia. Sprague-Dawley male rats, weighing 220-250 g at the time of recruitment were randomly divided into 7 groups (n = 4 per group), the control normoxia group was exposed to room air, while the hypoxia group were caged in a plexiglass hypoxic chamber (8%O2 and 92% N2) for 1, 3, 7, 14, 21, and 28 days, respectively. RESULTS: Our data clearly showed that plasma BNP-45 and ventricular BNP-45 mRNA concentration were markedly increased which reached its peak on day 21 after treatment. CONCLUSION: Regulation of BNP-45 gene expression occurred at transcription as well as post-transcription level. Systemic chronic hypoxia could result in heart failure, especially when the hypoxia is severe and prolonged.
AIM: To investigate the expression of B-type natriuretic peptide-45 (BNP-45) gene which was induced by systemic chronic hypoxia, and whether these changes would be different from BNP-45 protein in the plasma and its mRNA in the ventricular myocardial. This study also aimed to test the hypothesis that systemic chronic hypoxia may cause heart failure. METHODS: Although clinical use of BNP as a biomarker in heart failure is increasing, the specificity of BNP for heart failure is not robust, suggesting that other mechanisms beyond simple ventricular stretch stimulate BNP release. Plasma BNP levels were markedly increased in patients with coronary artery disease but without concomitant left ventricular dysfunction. Thus, elevated BNP levels do not necessarily reflect heart failure but may also result from cardiac ischemia. Sprague-Dawley male rats, weighing 220-250 g at the time of recruitment were randomly divided into 7 groups (n = 4 per group), the control normoxia group was exposed to room air, while the hypoxia group were caged in a plexiglass hypoxic chamber (8%O2 and 92% N2) for 1, 3, 7, 14, 21, and 28 days, respectively. RESULTS: Our data clearly showed that plasma BNP-45 and ventricular BNP-45 mRNA concentration were markedly increased which reached its peak on day 21 after treatment. CONCLUSION: Regulation of BNP-45 gene expression occurred at transcription as well as post-transcription level. Systemic chronic hypoxia could result in heart failure, especially when the hypoxia is severe and prolonged.