Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure

Objective: We evaluated the hypothesis that the development of renal dysfunction and congestive heart failure (CHF) caused by volume overload in rats with angiotensin II (ANG II)-dependent hypertension is associated with altered renal vascular responsiveness to ANG II and to epoxyeicosatrienoic acid...

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Main Authors: Šárka Vacková, Soňa Kikerlová, Vojtěch Melenovsky, František Kolář, John D. Imig, Elzbieta Kompanowska-Jezierska, Janusz Sadowski, Luděk Červenka
Format: Article
Language:English
Published: Karger Publishers 2019-08-01
Series:Kidney & Blood Pressure Research
Subjects:
Online Access:https://www.karger.com/Article/FullText/501688
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author Šárka Vacková
Soňa Kikerlová
Vojtěch Melenovsky
František Kolář
John D. Imig
Elzbieta Kompanowska-Jezierska
Janusz Sadowski
Luděk Červenka
author_facet Šárka Vacková
Soňa Kikerlová
Vojtěch Melenovsky
František Kolář
John D. Imig
Elzbieta Kompanowska-Jezierska
Janusz Sadowski
Luděk Červenka
author_sort Šárka Vacková
collection DOAJ
description Objective: We evaluated the hypothesis that the development of renal dysfunction and congestive heart failure (CHF) caused by volume overload in rats with angiotensin II (ANG II)-dependent hypertension is associated with altered renal vascular responsiveness to ANG II and to epoxyeicosatrienoic acids (EETs). Methods: Ren-2 transgenic rats (TGRs) were used as a model of ANG II-dependent hypertension. CHF was induced by volume overload achieved by the creation of the aorto-caval fistula (ACF). Renal blood flow (RBF) responses were determined to renal arterial administration of ANG II, native 11,12-EET, an analog of 14,15-EETs (EET-A), norepinephrine (NE), acetylcholine (Ach) and bradykinin (Bk) in healthy (i.e., sham-operated) TGR and ACF TGR (5 weeks after ACF creation). Results: Selective intrarenal administration of neither vasoactive drug altered mean arterial pressure in any group. Administration of ANG II caused greater decreases in RBF in ACF TGR than in sham-operated TGR, whereas after administration of NE the respective decreases were comparable in the 2 groups. Administration of Ach and Bk elicited significantly higher RBF increases in ACF TGR as compared with sham-operated TGR. In contrast, administration of 11,12-EET and EET-A caused significantly smaller RBF increases in ACF TGR than in sham-operated TGR. Conclusion: The findings show that 5 weeks after creation of ACF, the TGR exhibit exaggerated renal vasoconstrictor responses to ANG II and reduced renal vasodilatory responses to EETs, suggesting that both these alterations might play an important role in the development of renal dysfunction in this model of CHF.
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spelling doaj.art-860926ce4fb8419a9ce934fde24c6d6f2022-12-22T01:27:40ZengKarger PublishersKidney & Blood Pressure Research1420-40961423-01432019-08-0144479280910.1159/000501688501688Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart FailureŠárka VackováSoňa KikerlováVojtěch MelenovskyFrantišek KolářJohn D. ImigElzbieta Kompanowska-JezierskaJanusz SadowskiLuděk ČervenkaObjective: We evaluated the hypothesis that the development of renal dysfunction and congestive heart failure (CHF) caused by volume overload in rats with angiotensin II (ANG II)-dependent hypertension is associated with altered renal vascular responsiveness to ANG II and to epoxyeicosatrienoic acids (EETs). Methods: Ren-2 transgenic rats (TGRs) were used as a model of ANG II-dependent hypertension. CHF was induced by volume overload achieved by the creation of the aorto-caval fistula (ACF). Renal blood flow (RBF) responses were determined to renal arterial administration of ANG II, native 11,12-EET, an analog of 14,15-EETs (EET-A), norepinephrine (NE), acetylcholine (Ach) and bradykinin (Bk) in healthy (i.e., sham-operated) TGR and ACF TGR (5 weeks after ACF creation). Results: Selective intrarenal administration of neither vasoactive drug altered mean arterial pressure in any group. Administration of ANG II caused greater decreases in RBF in ACF TGR than in sham-operated TGR, whereas after administration of NE the respective decreases were comparable in the 2 groups. Administration of Ach and Bk elicited significantly higher RBF increases in ACF TGR as compared with sham-operated TGR. In contrast, administration of 11,12-EET and EET-A caused significantly smaller RBF increases in ACF TGR than in sham-operated TGR. Conclusion: The findings show that 5 weeks after creation of ACF, the TGR exhibit exaggerated renal vasoconstrictor responses to ANG II and reduced renal vasodilatory responses to EETs, suggesting that both these alterations might play an important role in the development of renal dysfunction in this model of CHF.https://www.karger.com/Article/FullText/501688Congestive heart failureHypertensionAorto-caval fistulaRenal blood flowRenal dysfunctionRenal vascular reactivityAngiotensin IIEpoxyeicosatrienoic acidNorepinephrineAcetylcholineBradykinin
spellingShingle Šárka Vacková
Soňa Kikerlová
Vojtěch Melenovsky
František Kolář
John D. Imig
Elzbieta Kompanowska-Jezierska
Janusz Sadowski
Luděk Červenka
Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure
Kidney & Blood Pressure Research
Congestive heart failure
Hypertension
Aorto-caval fistula
Renal blood flow
Renal dysfunction
Renal vascular reactivity
Angiotensin II
Epoxyeicosatrienoic acid
Norepinephrine
Acetylcholine
Bradykinin
title Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure
title_full Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure
title_fullStr Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure
title_full_unstemmed Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure
title_short Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure
title_sort altered renal vascular responsiveness to vasoactive agents in rats with angiotensin ii dependent hypertension and congestive heart failure
topic Congestive heart failure
Hypertension
Aorto-caval fistula
Renal blood flow
Renal dysfunction
Renal vascular reactivity
Angiotensin II
Epoxyeicosatrienoic acid
Norepinephrine
Acetylcholine
Bradykinin
url https://www.karger.com/Article/FullText/501688
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