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Augmented expression of cardiac atrial natriuretic peptide system in hypertensive rats.

The present study was aimed at investigating the regulation of atrial natriuretic peptide (ANP) system in association with either enhanced or attenuated activity of the renin-angiotensin system (RAS). The cardiac tissue mRNA and peptide levels of ANP were measured in rats with two-kidney, one clip (...

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Detalles Bibliográficos
Autores principales: An, M. R., Chung, Y. J., Kang, D. G., Nam, S. C., Lee, J.
Formato: Texto
Lenguaje:English
Publicado: Korean Academy of Medical Sciences 1999
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3054466/
https://www.ncbi.nlm.nih.gov/pubmed/10576144
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author An, M. R.
Chung, Y. J.
Kang, D. G.
Nam, S. C.
Lee, J.
author_facet An, M. R.
Chung, Y. J.
Kang, D. G.
Nam, S. C.
Lee, J.
author_sort An, M. R.
collection PubMed
description The present study was aimed at investigating the regulation of atrial natriuretic peptide (ANP) system in association with either enhanced or attenuated activity of the renin-angiotensin system (RAS). The cardiac tissue mRNA and peptide levels of ANP were measured in rats with two-kidney, one clip (2K1C) or deoxycorticosterone acetate (DOCA)-salt hypertension. Plasma renin concentration was increased in 2K1C hypertension along with increases of renin mRNA and protein contents in the clipped kidney. On the contrary, it was suppressed in DOCA-salt hypertension along with decreases of renin mRNA and protein contents in the remaining kidney. The plasma ANP concentration was similarly increased in both models of hypertension. The cardiac tissue ANP contents were not significantly changed, but the tissue ANP mRNA levels were upregulated in the hypertrophied heart in these two models of hypertension. It is suggested that the cardiac ANP system is transcriptionally enhanced by cardiac hypertrophy associated with hypertension, independent of the systemic RAS.
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spelling pubmed-30544662011-03-15 Augmented expression of cardiac atrial natriuretic peptide system in hypertensive rats. An, M. R. Chung, Y. J. Kang, D. G. Nam, S. C. Lee, J. J Korean Med Sci Research Article The present study was aimed at investigating the regulation of atrial natriuretic peptide (ANP) system in association with either enhanced or attenuated activity of the renin-angiotensin system (RAS). The cardiac tissue mRNA and peptide levels of ANP were measured in rats with two-kidney, one clip (2K1C) or deoxycorticosterone acetate (DOCA)-salt hypertension. Plasma renin concentration was increased in 2K1C hypertension along with increases of renin mRNA and protein contents in the clipped kidney. On the contrary, it was suppressed in DOCA-salt hypertension along with decreases of renin mRNA and protein contents in the remaining kidney. The plasma ANP concentration was similarly increased in both models of hypertension. The cardiac tissue ANP contents were not significantly changed, but the tissue ANP mRNA levels were upregulated in the hypertrophied heart in these two models of hypertension. It is suggested that the cardiac ANP system is transcriptionally enhanced by cardiac hypertrophy associated with hypertension, independent of the systemic RAS. Korean Academy of Medical Sciences 1999-10 /pmc/articles/PMC3054466/ /pubmed/10576144 Text en
spellingShingle Research Article
An, M. R.
Chung, Y. J.
Kang, D. G.
Nam, S. C.
Lee, J.
Augmented expression of cardiac atrial natriuretic peptide system in hypertensive rats.
title Augmented expression of cardiac atrial natriuretic peptide system in hypertensive rats.
title_full Augmented expression of cardiac atrial natriuretic peptide system in hypertensive rats.
title_fullStr Augmented expression of cardiac atrial natriuretic peptide system in hypertensive rats.
title_full_unstemmed Augmented expression of cardiac atrial natriuretic peptide system in hypertensive rats.
title_short Augmented expression of cardiac atrial natriuretic peptide system in hypertensive rats.
title_sort augmented expression of cardiac atrial natriuretic peptide system in hypertensive rats.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3054466/
https://www.ncbi.nlm.nih.gov/pubmed/10576144
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