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dc.contributorDepartment of Health Technology and Informatics-
dc.creatorZaw, AM-
dc.creatorSekar, R-
dc.creatorMak, SOK-
dc.creatorLaw, HKW-
dc.creatorChow, BKC-
dc.publisherNature Publishing Groupen_US
dc.rightsOpen Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Cre-ative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not per-mitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit
dc.rights© The Author(s) 2019en_US
dc.rightsThe following publication Zaw, A.M., Sekar, R., Mak, S.O.K. et al. Loss of secretin results in systemic and pulmonary hypertension with cardiopulmonary pathologies in mice. Sci Rep 9, 14211 (2019), 1-13 is available at
dc.titleLoss of secretin results in systemic and pulmonary hypertension with cardiopulmonary pathologies in miceen_US
dc.typeJournal/Magazine Articleen_US
dcterms.abstractMore than 1 billion people globally are suffering from hypertension, which is a long-term incurable medical condition that can further lead to dangerous complications and death if left untreated. In earlier studies, the brain-gut peptide secretin (SCT) was found to be able to control blood pressure by its cardiovascular and pulmonary effects. For example, serum SCT in patients with congestive heart failure was one-third of the normal level. These observations strongly suggest that SCT has a causal role in blood pressure control, and in this report, we used constitutive SCT knockout (SCT-/-) mice and control C57BL/6N mice to investigate differences in the morphology, function, underlying mechanisms and response to SCT treatment. We found that SCT-/- mice suffer from systemic and pulmonary hypertension with increased fibrosis in the lungs and heart. Small airway remodelling and pulmonary inflammation were also found in SCT-/- mice. Serum NO and VEGF levels were reduced and plasma aldosterone levels were increased in SCT-/- mice. Elevated cardiac aldosterone and decreased VEGF in the lungs were observed in the SCT-/- mice. More interestingly, SCT replacement in SCT-/- mice could prevent the development of heart and lung pathologies compared to the untreated group. Taken together, we comprehensively demonstrated the critical role of SCT in the cardiovascular and pulmonary systems and provide new insight into the potential role of SCT in the pathological development of cardiopulmonary and cardiovascular diseases.-
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationScientific reports, 2 Oct. 2019, v. 9, 14211, p. 1-13-
dcterms.isPartOfScientific reports-
dc.description.validate202002 bcrc-
dc.description.oaVersion of Recorden_US
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