Detail
Článek
Článek online
FT
Medvik - BMČ
  • Je něco špatně v tomto záznamu ?

Effect of Ivabradine on a Hypertensive Heart and the Renin-Angiotensin-Aldosterone System in L-NAME-Induced Hypertension

F. Simko, T. Baka, M. Poglitsch, K. Repova, S. Aziriova, K. Krajcirovicova, S. Zorad, M. Adamcova, L. Paulis,

. 2018 ; 19 (10) : . [pub] 20181003

Jazyk angličtina Země Švýcarsko

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc19012306

Ivabradine, the selective inhibitor of the If current in the sinoatrial node, exerts cardiovascular protection by its bradycardic effect and potentially pleiotropic actions. However, there is a shortage of data regarding ivabradine's interaction with the renin-angiotensin-aldosterone system (RAAS). This study investigated whether ivabradine is able to protect a hypertensive heart in the model of L-NAME-induced hypertension and to interfere with the RAAS. Four groups (n = 10/group) of adult male Wistar rats were treated as follows for four weeks: control, ivabradine (10 mg/kg/day), L-NAME (40 mg/kg/day), and L-NAME plus ivabradine. L-NAME administration increased systolic blood pressure (SBP) and left ventricular (LV) weight, enhanced hydroxyproline concentration in the LV, and deteriorated the systolic and diastolic LV function. Ivabradine reduced heart rate (HR) and SBP, and improved the LV function. The serum concentrations of angiotensin Ang 1−8 (Ang II), Ang 1−5, Ang 1−7, Ang 1−10, Ang 2−8, and Ang 3−8 were decreased in the L-NAME group and ivabradine did not modify them. The serum concentration of aldosterone and the aldosterone/Ang II ratio were enhanced by L-NAME and ivabradine reduced these changes. We conclude that ivabradine improved the LV function of the hypertensive heart in L-NAME-induced hypertension. The protective effect of ivabradine might have been associated with the reduction of the aldosterone level.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc19012306
003      
CZ-PrNML
005      
20231121102314.0
007      
ta
008      
190405s2018 sz f 000 0|eng||
009      
AR
024    7_
$a 10.3390/ijms19103017 $2 doi
035    __
$a (PubMed)30282928
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a sz
100    1_
$a Simko, Fedor $u Institute of Pathophysiology, Faculty of Medicine, Comenius University, Sasinkova 4, 81108 Bratislava, Slovakia. fedor.simko@fmed.uniba.sk. 3rd Department of Internal Medicine, Faculty of Medicine, Comenius University, 83305 Bratislava, Slovakia. fedor.simko@fmed.uniba.sk. Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, 84505 Bratislava, Slovakia. fedor.simko@fmed.uniba.sk.
245    10
$a Effect of Ivabradine on a Hypertensive Heart and the Renin-Angiotensin-Aldosterone System in L-NAME-Induced Hypertension / $c F. Simko, T. Baka, M. Poglitsch, K. Repova, S. Aziriova, K. Krajcirovicova, S. Zorad, M. Adamcova, L. Paulis,
520    9_
$a Ivabradine, the selective inhibitor of the If current in the sinoatrial node, exerts cardiovascular protection by its bradycardic effect and potentially pleiotropic actions. However, there is a shortage of data regarding ivabradine's interaction with the renin-angiotensin-aldosterone system (RAAS). This study investigated whether ivabradine is able to protect a hypertensive heart in the model of L-NAME-induced hypertension and to interfere with the RAAS. Four groups (n = 10/group) of adult male Wistar rats were treated as follows for four weeks: control, ivabradine (10 mg/kg/day), L-NAME (40 mg/kg/day), and L-NAME plus ivabradine. L-NAME administration increased systolic blood pressure (SBP) and left ventricular (LV) weight, enhanced hydroxyproline concentration in the LV, and deteriorated the systolic and diastolic LV function. Ivabradine reduced heart rate (HR) and SBP, and improved the LV function. The serum concentrations of angiotensin Ang 1−8 (Ang II), Ang 1−5, Ang 1−7, Ang 1−10, Ang 2−8, and Ang 3−8 were decreased in the L-NAME group and ivabradine did not modify them. The serum concentration of aldosterone and the aldosterone/Ang II ratio were enhanced by L-NAME and ivabradine reduced these changes. We conclude that ivabradine improved the LV function of the hypertensive heart in L-NAME-induced hypertension. The protective effect of ivabradine might have been associated with the reduction of the aldosterone level.
650    _2
$a aldosteron $x krev $7 D000450
650    _2
$a angiotensiny $x krev $7 D000809
650    _2
$a zvířata $7 D000818
650    _2
$a biologické markery $7 D015415
650    _2
$a krevní tlak $x účinky léků $7 D001794
650    _2
$a kardiovaskulární látky $x farmakologie $7 D002317
650    _2
$a kolagen $x metabolismus $7 D003094
650    _2
$a modely nemocí na zvířatech $7 D004195
650    _2
$a echokardiografie $7 D004452
650    _2
$a hydroxyprolin $x krev $x metabolismus $7 D006909
650    _2
$a hypertenze $x diagnóza $x etiologie $x metabolismus $x patofyziologie $7 D006973
650    _2
$a ivabradin $x farmakologie $7 D000077550
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a NG-nitroargininmethylester $x škodlivé účinky $7 D019331
650    _2
$a krysa rodu Rattus $7 D051381
650    _2
$a renin $x krev $7 D012083
650    _2
$a renin-angiotensin systém $x účinky léků $7 D012084
650    _2
$a funkce levé komory srdeční $x účinky léků $7 D016277
655    _2
$a časopisecké články $7 D016428
700    1_
$a Baka, Tomáš, $u Institute of Pathophysiology, Faculty of Medicine, Comenius University, Sasinkova 4, 81108 Bratislava, Slovakia. tomasko.baka@gmail.com. $d 1989- $7 xx0263984
700    1_
$a Poglitsch, Marko $u Attoquant Diagnostics, 1030 Vienna, Austria. marko.poglitsch@attoquant.com.
700    1_
$a Repová, Kristína, $u Institute of Pathophysiology, Faculty of Medicine, Comenius University, Sasinkova 4, 81108 Bratislava, Slovakia. repova.k@gmail.com. $d 1984- $7 xx0264906
700    1_
$a Aziriova, Silvia $u Institute of Pathophysiology, Faculty of Medicine, Comenius University, Sasinkova 4, 81108 Bratislava, Slovakia. silvia.aziriova@gmail.com.
700    1_
$a Krajcirovicova, Kristina $u Institute of Pathophysiology, Faculty of Medicine, Comenius University, Sasinkova 4, 81108 Bratislava, Slovakia. krikratina@gmail.com.
700    1_
$a Zorad, Štefan, $d 1956- $u Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, 84505 Bratislava, Slovakia. stefan.zorad@savba.sk. $7 xx0310348
700    1_
$a Adamcova, Michaela $u Department of Physiology, School of Medicine, Charles University, 50003 Hradec Kralove, Czech Republic. adamcova@lfhk.cuni.cz.
700    1_
$a Paulis, Ludovit $u Institute of Pathophysiology, Faculty of Medicine, Comenius University, Sasinkova 4, 81108 Bratislava, Slovakia. ludovit.paulis@gmail.com. Institute of Normal and Pathological Physiology, Center for Experimental Medicine, Slovak Academy of Sciences, 81371 Bratislava, Slovakia. ludovit.paulis@gmail.com.
773    0_
$w MED00176142 $t International journal of molecular sciences $x 1422-0067 $g Roč. 19, č. 10 (2018)
856    41
$u https://pubmed.ncbi.nlm.nih.gov/30282928 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y a $z 0
990    __
$a 20190405 $b ABA008
991    __
$a 20231121102311 $b ABA008
999    __
$a ok $b bmc $g 1391616 $s 1050611
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2018 $b 19 $c 10 $e 20181003 $i 1422-0067 $m International journal of molecular sciences $n Int J Mol Sci $x MED00176142
LZP    __
$a Pubmed-20190405

Najít záznam

Citační ukazatele

Možnosti archivace