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Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure
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SYSNO ASEP 0509188 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure Author(s) Vacková, Š. (CZ)
Kikerlová, S. (CZ)
Melenovský, V. (CZ)
Kolář, František (FGU-C) RID, ORCID, SAI
Imig, J. D. (US)
Kompanowska - Jezierska, E. (PL)
Sadowski, J. (PL)
Červenka, L. (CZ)Source Title Kidney & Blood Pressure Research. - : Karger - ISSN 1420-4096
Roč. 44, č. 4 (2019), s. 792-809Number of pages 18 s. Language eng - English Country CH - Switzerland Keywords congestive heart failure ; hypertension ; aorto-caval fistula ; renal blood flow ; renal dysfunction ; renal vascular reactivity ; angiotensin II ; epoxyeicosatrienoic acid Subject RIV FA - Cardiovascular Diseases incl. Cardiotharic Surgery OECD category Cardiac and Cardiovascular systems R&D Projects NV18-02-00053 GA MZd - Ministry of Health (MZ) Method of publishing Open access Institutional support FGU-C - RVO:67985823 UT WOS 000483857700028 EID SCOPUS 85071709898 DOI 10.1159/000501688 Annotation 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. Workplace Institute of Physiology Contact Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Year of Publishing 2020 Electronic address https://doi.org/10.1159/000501688
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