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Cardiorenal and endocrine effects of synthetic canine BNP1‐32 in dogs with compensated congestive heart failure caused by myxomatous mitral valve disease

BACKGROUND: The effects of synthetic brain natriuretic peptide (BNP1‐32) on cardiorenal and renin angiotensin aldosterone system in dogs with naturally occurring congestive heart failure (CHF) are unknown. OBJECTIVES: To evaluate the cardiorenal and endocrine effects of SC administered synthetic can...

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Autores principales: Yata, Mariko, Kooistra, Hans S., Beijerink, Niek J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons, Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6430907/
https://www.ncbi.nlm.nih.gov/pubmed/30703246
http://dx.doi.org/10.1111/jvim.15416
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author Yata, Mariko
Kooistra, Hans S.
Beijerink, Niek J.
author_facet Yata, Mariko
Kooistra, Hans S.
Beijerink, Niek J.
author_sort Yata, Mariko
collection PubMed
description BACKGROUND: The effects of synthetic brain natriuretic peptide (BNP1‐32) on cardiorenal and renin angiotensin aldosterone system in dogs with naturally occurring congestive heart failure (CHF) are unknown. OBJECTIVES: To evaluate the cardiorenal and endocrine effects of SC administered synthetic canine BNP1‐32, with or without furosemide, in dogs with CHF caused by myxomatous mitral valve disease (MMVD). ANIMALS: Seven client‐owned male dogs with compensated American College of Veterinary Internal Medicine stage C CHF caused by MMVD on chronic treatment with furosemide, benazepril, and pimobendan. METHODS: A single‐dose, crossover, pilot study. Each dog received a dose of BNP1‐32 (5 μg/kg), furosemide (2 mg/kg), and both BNP1‐32/furosemide (5 μg/kg and 2 mg/kg, respectively) SC with a 2‐week washout period among each treatment. Between‐ and within‐treatment effects were evaluated using linear mixed modeling with restricted maximum likelihood estimation and evaluation of least square differences. RESULTS: Rapid absorption of BNP1‐32 and a corresponding rise in urinary cyclic guanosine monophosphate excretion was observed at 1‐2 hours after any treatment containing BNP1‐32 (P < .05). However, BNP1‐32 did not influence measured cardiorenal variables. Plasma aldosterone concentrations were below quantifiable levels in majority of the samples. CONCLUSIONS AND CLINICAL IMPORTANCE: No beneficial cardiorenal effects were detected. It is possible that dogs with chronic CHF have a reduction in natriuretic peptide responsiveness.
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spelling pubmed-64309072019-04-04 Cardiorenal and endocrine effects of synthetic canine BNP1‐32 in dogs with compensated congestive heart failure caused by myxomatous mitral valve disease Yata, Mariko Kooistra, Hans S. Beijerink, Niek J. J Vet Intern Med SMALL ANIMAL BACKGROUND: The effects of synthetic brain natriuretic peptide (BNP1‐32) on cardiorenal and renin angiotensin aldosterone system in dogs with naturally occurring congestive heart failure (CHF) are unknown. OBJECTIVES: To evaluate the cardiorenal and endocrine effects of SC administered synthetic canine BNP1‐32, with or without furosemide, in dogs with CHF caused by myxomatous mitral valve disease (MMVD). ANIMALS: Seven client‐owned male dogs with compensated American College of Veterinary Internal Medicine stage C CHF caused by MMVD on chronic treatment with furosemide, benazepril, and pimobendan. METHODS: A single‐dose, crossover, pilot study. Each dog received a dose of BNP1‐32 (5 μg/kg), furosemide (2 mg/kg), and both BNP1‐32/furosemide (5 μg/kg and 2 mg/kg, respectively) SC with a 2‐week washout period among each treatment. Between‐ and within‐treatment effects were evaluated using linear mixed modeling with restricted maximum likelihood estimation and evaluation of least square differences. RESULTS: Rapid absorption of BNP1‐32 and a corresponding rise in urinary cyclic guanosine monophosphate excretion was observed at 1‐2 hours after any treatment containing BNP1‐32 (P < .05). However, BNP1‐32 did not influence measured cardiorenal variables. Plasma aldosterone concentrations were below quantifiable levels in majority of the samples. CONCLUSIONS AND CLINICAL IMPORTANCE: No beneficial cardiorenal effects were detected. It is possible that dogs with chronic CHF have a reduction in natriuretic peptide responsiveness. John Wiley & Sons, Inc. 2019-01-31 2019 /pmc/articles/PMC6430907/ /pubmed/30703246 http://dx.doi.org/10.1111/jvim.15416 Text en © 2019 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle SMALL ANIMAL
Yata, Mariko
Kooistra, Hans S.
Beijerink, Niek J.
Cardiorenal and endocrine effects of synthetic canine BNP1‐32 in dogs with compensated congestive heart failure caused by myxomatous mitral valve disease
title Cardiorenal and endocrine effects of synthetic canine BNP1‐32 in dogs with compensated congestive heart failure caused by myxomatous mitral valve disease
title_full Cardiorenal and endocrine effects of synthetic canine BNP1‐32 in dogs with compensated congestive heart failure caused by myxomatous mitral valve disease
title_fullStr Cardiorenal and endocrine effects of synthetic canine BNP1‐32 in dogs with compensated congestive heart failure caused by myxomatous mitral valve disease
title_full_unstemmed Cardiorenal and endocrine effects of synthetic canine BNP1‐32 in dogs with compensated congestive heart failure caused by myxomatous mitral valve disease
title_short Cardiorenal and endocrine effects of synthetic canine BNP1‐32 in dogs with compensated congestive heart failure caused by myxomatous mitral valve disease
title_sort cardiorenal and endocrine effects of synthetic canine bnp1‐32 in dogs with compensated congestive heart failure caused by myxomatous mitral valve disease
topic SMALL ANIMAL
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6430907/
https://www.ncbi.nlm.nih.gov/pubmed/30703246
http://dx.doi.org/10.1111/jvim.15416
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