Progression of hypertension and kidney disease in aging fawn-hooded rats is mediated by enhanced influence of renin-angiotensin system and suppression of nitric oxide system and epoxyeicosanoids
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023001%3A_____%2F16%3A00060087" target="_blank" >RIV/00023001:_____/16:00060087 - isvavai.cz</a>
Alternative codes found
RIV/00216208:11130/16:10328553 RIV/00216208:11310/16:10328553
Result on the web
<a href="http://www.tandfonline.com/doi/full/10.1080/10641963.2016.1182182?scroll=top&needAccess=true" target="_blank" >http://www.tandfonline.com/doi/full/10.1080/10641963.2016.1182182?scroll=top&needAccess=true</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1080/10641963.2016.1182182" target="_blank" >10.1080/10641963.2016.1182182</a>
Alternative languages
Result language
angličtina
Original language name
Progression of hypertension and kidney disease in aging fawn-hooded rats is mediated by enhanced influence of renin-angiotensin system and suppression of nitric oxide system and epoxyeicosanoids
Original language description
The fawn-hooded hypertensive (FHH) rat serves as a genetic model of spontaneous hypertension associated with glomerular hyperfiltration and proteinuria. However, the knowledge of the natural course of hypertension and kidney disease in FHH rats remains fragmentary and the underlying pathophysiological mechanisms are unclear. In this study, over the animals' lifetime, we followed the survival rate, blood pressure (telemetry), indices of kidney damage, the activity of renin-angiotensin (RAS) and nitric oxide (NO) systems, and CYP450-epoxygenase products (EETs). Compared to normotensive controls, no elevation of plasma and renal RAS was observed in prehypertensive and hypertensive FHH rats; however, RAS inhibition significantly reduced systolic blood pressure (137 +/- 9 to 116 +/- 8, and 159 +/- 8 to 126 +/- 4 mmHg, respectively) and proteinuria (62 +/- 2 to 37 +/- 3, and 132 +/- 8 to 87 +/- 5 mg/day, respectively). Moreover, pharmacological RAS inhibition reduced angiotensin (ANG) II and increased ANG 1-7 in the kidney and thereby may have delayed the progression of kidney disease. Furthermore, renal NO and EETs declined in the aging FHH rats but not in the control strain. The present results, especially the demonstration of exaggerated vascular responsiveness to ANG II, indicate that RAS may contribute to the development of hypertension and kidney disease in FHH rats. The activity of factors opposing the development of hypertension and protecting the kidney declined with age in this model. Therefore, therapeutic enhancement of this activity besides RAS inhibition could be attempted in the therapy of human hypertension associated with kidney disease.
Czech name
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Czech description
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Classification
Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
FA - Cardiovascular diseases including cardio-surgery
OECD FORD branch
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Result continuities
Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2016
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Clinical and experimental hypertension
ISSN
1064-1963
e-ISSN
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Volume of the periodical
38
Issue of the periodical within the volume
7
Country of publishing house
US - UNITED STATES
Number of pages
8
Pages from-to
644-651
UT code for WoS article
000386114700013
EID of the result in the Scopus database
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