Abstract
Specific relaxin binding sites present in the heart and blood vessels and chronotropic and inotropic responses to relaxin have been documented [1,2] implying that relaxin exerts cardiovascular properties. The circulation levels of endogenous relaxin, however, are extremely low whilst the doses of relaxin used for demonstrating pharmacological effects are very high. Thus, the biological effects of relaxin on the cardiovascular system remain unclear. We have studied the cardiac phenotype of 15~20 month old male and female mice with disruption of the relaxin gene (−/−) [3], in comparison with wild-type (+/+) and heterozygous (+/−), generated by Zhao et al. at the Howard Florey Institute [3]. Under anaesthetized conditions, transthoracic echocardiography was conducted using a HP 5500 echo machine with a 15MHz linear probe, followed by cardiac catheterization via the right carotid artery using a 1.4F Millar micro-tip pressure transducer catheter [4]. Organ weights were obtained and myocardial content of collagen was measured by determining concentration of hydroxyproline in the left ventricle (LV). Each group had 8 to 10 mice.
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© 2001 Springer Science+Business Media Dordrecht
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Du, XJ., Zhao, L., Gao, XM., Tregear, G.W. (2001). Cardiovascular phenotypes of relaxin knockout mice: Importance of gender. In: Tregear, G.W., Ivell, R., Bathgate, R.A., Wade, J.D. (eds) Relaxin 2000. Springer, Dordrecht. https://doi.org/10.1007/978-94-017-2877-5_27
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DOI: https://doi.org/10.1007/978-94-017-2877-5_27
Publisher Name: Springer, Dordrecht
Print ISBN: 978-90-481-5845-4
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