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McCarthy JC, Aronovitz M, DuPont JJ, et al. Short-Term Administration of Serelaxin Produces Predominantly Vascular Benefits in the Angiotensin II/L-NAME Chronic Heart Failure Model. JACC Basic Transl Sci. 2017;2(3):285-296doi: 10.1016/j.jacbts.2017.03.011.
McCarthy, J. C., Aronovitz, M., DuPont, J. J., Calamaras, T. D., Jaffe, I. Z., & Blanton, R. M. (2017). Short-Term Administration of Serelaxin Produces Predominantly Vascular Benefits in the Angiotensin II/L-NAME Chronic Heart Failure Model. JACC. Basic to translational science, 2(3), 285-296. https://doi.org/10.1016/j.jacbts.2017.03.011
McCarthy, Joseph C, et al. "Short-Term Administration of Serelaxin Produces Predominantly Vascular Benefits in the Angiotensin II/L-NAME Chronic Heart Failure Model." JACC. Basic to translational science vol. 2,3 (2017): 285-296. doi: https://doi.org/10.1016/j.jacbts.2017.03.011
McCarthy JC, Aronovitz M, DuPont JJ, Calamaras TD, Jaffe IZ, Blanton RM. Short-Term Administration of Serelaxin Produces Predominantly Vascular Benefits in the Angiotensin II/L-NAME Chronic Heart Failure Model. JACC Basic Transl Sci. 2017 Jun 26;2(3):285-296. doi: 10.1016/j.jacbts.2017.03.011. eCollection 2017 Jun. PMID: 30062150; PMCID: PMC6034497.
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JACC Basic Transl Sci. 2017 Jun 26;2(3):285-296. doi: 10.1016/j.jacbts.2017.03.011. eCollection 2017 Jun.

Short-Term Administration of Serelaxin Produces Predominantly Vascular Benefits in the Angiotensin II/L-NAME Chronic Heart Failure Model.

JACC. Basic to translational science

Joseph C McCarthy, Mark Aronovitz, Jennifer J DuPont, Timothy D Calamaras, Iris Z Jaffe, Robert M Blanton

Affiliations

  1. Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts.

PMID: 30062150 PMCID: PMC6034497 DOI: 10.1016/j.jacbts.2017.03.011

Abstract

In patients hospitalized with acute heart failure, temporary serelaxin infusion reduced 6-month mortality through unknown mechanisms. This study therefore explored the cardiovascular effects of temporary serelaxin administration in mice subjected to the angiotensin II (AngII)/L-NG-nitroarginine methyl ester (L-NAME) heart failure model, both during serelaxin infusion and 19 days post-serelaxin infusion. Serelaxin administration did not alter AngII/L-NAME-induced cardiac hypertrophy, geometry, or dysfunction. However, serelaxin-treated mice had reduced perivascular left ventricular fibrosis and preserved left ventricular capillary density at both time points. Furthermore, resistance vessels from serelaxin-treated mice displayed decreased potassium chloride-induced constriction and reduced aortic fibrosis. These findings suggest that serelaxin improves outcomes in patients through vascular-protective effects.

Keywords: AngII, angiotensin II; HF, heart failure; L-NAME, L-NG-nitroarginine methyl ester; LV, left ventricular; SBP, systolic blood pressure; heart failure; relaxin; vascular function

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