-
Something wrong with this record ?
Effect of sacubitril/valsartan on the hypertensive heart in continuous light-induced and lactacystin-induced pre-hypertension: Interactions with the renin-angiotensin-aldosterone system
F. Simko, P. Stanko, K. Repova, T. Baka, K. Krajcirovicova, S. Aziriova, O. Domenig, S. Zorad, M. Adamcova, L. Paulis
Language English Country France
Document type Journal Article
- MeSH
- Acetylcysteine analogs & derivatives MeSH
- Aldosterone MeSH
- Aminobutyrates * MeSH
- Biphenyl Compounds pharmacology MeSH
- Fibrosis MeSH
- Drug Combinations MeSH
- Hypertension * drug therapy MeSH
- Hypertrophy, Left Ventricular MeSH
- Rats MeSH
- Rats, Wistar MeSH
- Prehypertension * MeSH
- Renin-Angiotensin System MeSH
- Renin MeSH
- Heart Failure * MeSH
- Stroke Volume MeSH
- Tetrazoles pharmacology therapeutic use MeSH
- Valsartan pharmacology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
This study investigated whether sacubitril/valsartan or valsartan are able to prevent left ventricular (LV) fibrotic remodelling and dysfunction in two experimental models of pre-hypertension induced by continuous light (24 hours/day) exposure or by chronic lactacystin treatment, and how this potential protection interferes with the renin-angiotensin-aldosterone system (RAAS). Nine groups of three-month-old male Wistar rats were treated for six weeks as follows: untreated controls (C), sacubitril/valsartan (ARNI), valsartan (Val), continuous light (24), continuous light plus sacubitril/valsartan (24+ARNI) or valsartan (24+Val), lactacystin (Lact), lactacystin plus sacubitil/valsartan (Lact+ARNI) or plus valsartan (Lact+Val). Both the 24 and Lact groups developed a mild but significant systolic blood pressure (SBP) increase, LV hypertrophy and fibrosis, as well as LV systolic and diastolic dysfunction. Yet, no changes in serum renin-angiotensin were observed either in the 24 or Lact groups, though aldosterone was increased in the Lact group compared to the controls. In both models, sacubitril/valsartan and valsartan reduced elevated SBP, LV hypertrophy and fibrosis and attenuated LV systolic and diastolic dysfunction. Sacubitril/valsartan and valsartan increased the serum levels of angiotensin (Ang) II, Ang III, Ang IV, Ang 1-5, Ang 1-7 in the 24 and Lact groups and reduced aldosterone in the Lact group. We conclude that both continuous light exposure and lactacystin treatment induced normal-to-low serum renin-angiotensin models of pre-hypertension, whereas aldosterone was increased in lactacystin-induced pre-hypertension. The protection by ARNI or valsartan in the hypertensive heart in either model was related to the Ang II blockade and the protective Ang 1-7, while in lactacystin-induced pre-hypertension this protection seems to be additionally related to the reduced aldosterone level.
References provided by Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc24006525
- 003
- CZ-PrNML
- 005
- 20240423155330.0
- 007
- ta
- 008
- 240412e20240311fr f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.1016/j.biopha.2024.116391 $2 doi
- 035 __
- $a (PubMed)38461685
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a fr
- 100 1_
- $a Simko, Fedor $u Institute of Pathophysiology, Faculty of Medicine, Comenius University, Bratislava 81108, Slovak Republic; 3rd Department of Internal Medicine, Faculty of Medicine, Comenius University, Bratislava 83305, Slovak Republic; Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava 84505, Slovak Republic. Electronic address: fedor.simko@fmed.uniba.sk
- 245 10
- $a Effect of sacubitril/valsartan on the hypertensive heart in continuous light-induced and lactacystin-induced pre-hypertension: Interactions with the renin-angiotensin-aldosterone system / $c F. Simko, P. Stanko, K. Repova, T. Baka, K. Krajcirovicova, S. Aziriova, O. Domenig, S. Zorad, M. Adamcova, L. Paulis
- 520 9_
- $a This study investigated whether sacubitril/valsartan or valsartan are able to prevent left ventricular (LV) fibrotic remodelling and dysfunction in two experimental models of pre-hypertension induced by continuous light (24 hours/day) exposure or by chronic lactacystin treatment, and how this potential protection interferes with the renin-angiotensin-aldosterone system (RAAS). Nine groups of three-month-old male Wistar rats were treated for six weeks as follows: untreated controls (C), sacubitril/valsartan (ARNI), valsartan (Val), continuous light (24), continuous light plus sacubitril/valsartan (24+ARNI) or valsartan (24+Val), lactacystin (Lact), lactacystin plus sacubitil/valsartan (Lact+ARNI) or plus valsartan (Lact+Val). Both the 24 and Lact groups developed a mild but significant systolic blood pressure (SBP) increase, LV hypertrophy and fibrosis, as well as LV systolic and diastolic dysfunction. Yet, no changes in serum renin-angiotensin were observed either in the 24 or Lact groups, though aldosterone was increased in the Lact group compared to the controls. In both models, sacubitril/valsartan and valsartan reduced elevated SBP, LV hypertrophy and fibrosis and attenuated LV systolic and diastolic dysfunction. Sacubitril/valsartan and valsartan increased the serum levels of angiotensin (Ang) II, Ang III, Ang IV, Ang 1-5, Ang 1-7 in the 24 and Lact groups and reduced aldosterone in the Lact group. We conclude that both continuous light exposure and lactacystin treatment induced normal-to-low serum renin-angiotensin models of pre-hypertension, whereas aldosterone was increased in lactacystin-induced pre-hypertension. The protection by ARNI or valsartan in the hypertensive heart in either model was related to the Ang II blockade and the protective Ang 1-7, while in lactacystin-induced pre-hypertension this protection seems to be additionally related to the reduced aldosterone level.
- 650 _2
- $a krysa rodu Rattus $7 D051381
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a mužské pohlaví $7 D008297
- 650 _2
- $a renin-angiotensin systém $7 D012084
- 650 _2
- $a renin $7 D012083
- 650 _2
- $a aldosteron $7 D000450
- 650 12
- $a prehypertenze $7 D058246
- 650 _2
- $a tetrazoly $x farmakologie $x terapeutické užití $7 D013777
- 650 _2
- $a potkani Wistar $7 D017208
- 650 _2
- $a valsartan $x farmakologie $7 D000068756
- 650 12
- $a hypertenze $x farmakoterapie $7 D006973
- 650 _2
- $a bifenylové sloučeniny $x farmakologie $7 D001713
- 650 12
- $a srdeční selhání $7 D006333
- 650 _2
- $a hypertrofie levé komory srdeční $7 D017379
- 650 _2
- $a fixní kombinace léků $7 D004338
- 650 _2
- $a fibróza $7 D005355
- 650 _2
- $a tepový objem $7 D013318
- 650 _2
- $a acetylcystein $x analogy a deriváty $7 D000111
- 650 12
- $a aminobutyráty $7 D000613
- 655 _2
- $a časopisecké články $7 D016428
- 700 1_
- $a Stanko, Peter $u Institute of Pathophysiology, Faculty of Medicine, Comenius University, Bratislava 81108, Slovak Republic; Department of Pneumology, Phthisiology and Functional Diagnostics, Slovak Medical University and Bratislava University Hospital, Bratislava, Slovak Republic
- 700 1_
- $a Repova, Kristina $u Institute of Pathophysiology, Faculty of Medicine, Comenius University, Bratislava 81108, Slovak Republic
- 700 1_
- $a Baka, Tomas $u Institute of Pathophysiology, Faculty of Medicine, Comenius University, Bratislava 81108, Slovak Republic
- 700 1_
- $a Krajcirovicova, Kristina $u Institute of Pathophysiology, Faculty of Medicine, Comenius University, Bratislava 81108, Slovak Republic
- 700 1_
- $a Aziriova, Silvia $u Institute of Pathophysiology, Faculty of Medicine, Comenius University, Bratislava 81108, Slovak Republic
- 700 1_
- $a Domenig, Oliver $u Attoquant Diagnostics, Vienna 1110, Austria
- 700 1_
- $a Zorad, Stefan $u Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava 84505, Slovak Republic
- 700 1_
- $a Adamcova, Michaela $u Department of Physiology, Charles University, Faculty of Medicine in Hradec Kralove, Hradec Kralove 50003, Czech Republic
- 700 1_
- $a Paulis, Ludovit $u Institute of Pathophysiology, Faculty of Medicine, Comenius University, Bratislava 81108, Slovak Republic; Centre of Experimental Medicine SAS, Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava 813 71, Slovak Republic
- 773 0_
- $w MED00005486 $t Biomedicine & pharmacotherapy $x 1950-6007 $g Roč. 173 (20240311), s. 116391
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/38461685 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y - $z 0
- 990 __
- $a 20240412 $b ABA008
- 991 __
- $a 20240423155327 $b ABA008
- 999 __
- $a ok $b bmc $g 2080861 $s 1216292
- BAS __
- $a 3
- BAS __
- $a PreBMC-MEDLINE
- BMC __
- $a 2024 $b 173 $c - $d 116391 $e 20240311 $i 1950-6007 $m Biomedicine & pharmacotherapy $n Biomed Pharmacother $x MED00005486
- LZP __
- $a Pubmed-20240412
