The Role of Renal Vascular Reactivity in the Development of Renal Dysfunction in Compensated and Decompensated Congestive Heart Failure
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11130%2F18%3A10387162" target="_blank" >RIV/00216208:11130/18:10387162 - isvavai.cz</a>
Alternative codes found
RIV/67985823:_____/18:00498679 RIV/00098892:_____/18:N0000121 RIV/00023001:_____/18:00077491
Result on the web
<a href="https://doi.org/10.1159/000495391" target="_blank" >https://doi.org/10.1159/000495391</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1159/000495391" target="_blank" >10.1159/000495391</a>
Alternative languages
Result language
angličtina
Original language name
The Role of Renal Vascular Reactivity in the Development of Renal Dysfunction in Compensated and Decompensated Congestive Heart Failure
Original language description
Background/Aims: Reduction of renal blood flow (RBF) is commonly thought to be a causative factor of renal dysfunction in congestive heart failure (CHF), but the exact mechanism of the renal hypoperfusion is not clear. Apart from the activation of neurohormonal systems controlling intrarenal vascular tone, the cause might be altered reactivity of the renal vasculature to endogenous vasoactive agents. Methods: To evaluate the role of this mechanism, we assessed by an ultrasonic transient-time flow probe maximum RBF responses to renal artery infusion of angiotensin II (ANG II), norepinephrine (NE) and acetylcholine (Ach) in healthy male rats and animals with compensated and decompensated CHF. CHF was induced by volume overload achieved by the creation of the aorto-caval fistula (ACF) in Hannover SpragueDawley rats. Results: Maximum responses in RBF to ANG II were similar in rats studied five weeks (compensated phase) and 20 weeks (decompensated phase) after ACF creation when compared to sham-operated rats. On the other hand, NE elicited larger maximum decreases in RBF in rats with CHF (five and 20 weeks post-ACF) than in sham-operated controls. We observed greater maximum vasodilatory responses to Ach only in rats with a compensated stage of CHF (five weeks post-ACF). Conclusion: Greater renal vasoconstrictor responsiveness to ANG II or reduced renal vasodilatation in response to Ach do not play a decisive role in the development of renal dysfunction in ACF rats with compensated and decompensated CHF. On the other hand, exaggerated renal vascular responsiveness to NE may be here a contributing causative factor, active in either CHF phase. (C) 2018 The Author(s) Published by S. Karger AG, Basel
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30105 - Physiology (including cytology)
Result continuities
Project
<a href="/en/project/NV18-02-00053" target="_blank" >NV18-02-00053: The role of renal dysfunction in the progression of congestive heart failure and its potential clinical implications: preclinical studies in animal models</a><br>
Continuities
S - Specificky vyzkum na vysokych skolach<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2018
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Kidney & Blood Pressure Research
ISSN
1420-4096
e-ISSN
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Volume of the periodical
43
Issue of the periodical within the volume
6
Country of publishing house
CH - SWITZERLAND
Number of pages
12
Pages from-to
1730-1741
UT code for WoS article
000455066300004
EID of the result in the Scopus database
2-s2.0-85057599199