• Something wrong with this record ?

Intrapulmonary activation of the angiotensin-converting enzyme type 2/angiotensin 1-7/G-protein-coupled Mas receptor axis attenuates pulmonary hypertension in Ren-2 transgenic rats exposed to chronic hypoxia

V. Hampl, J. Herget, J. Bíbová, A. Baňasová, Z. Husková, Z. Vaňourková, Š. Jíchová, P. Kujal, Z. Vernerová, J. Sadowski, L. Červenka

. 2015 ; 64 (1) : 25-38. [pub] 20140905

Language English Country Czech Republic

Document type Journal Article, Research Support, Non-U.S. Gov't

Persistent link   https://www.medvik.cz/link/bmc15040038

Grant support
NT14085 MZ0 CEP Register
NT13358 MZ0 CEP Register

The present study was performed to evaluate the role of intrapulmonary activity of the two axes of the renin-angiotensin system (RAS): vasoconstrictor angiotensin-converting enzyme (ACE)/angiotensin II (ANG II)/ANG II type 1 receptor (AT₁) axis, and vasodilator ACE type 2 (ACE2)/angiotensin 1-7 (ANG 1-7)/Mas receptor axis, in the development of hypoxic pulmonary hypertension in Ren-2 transgenic rats (TGR). Transgene-negative Hannover Sprague-Dawley (HanSD) rats served as controls. Both TGR and HanSD rats responded to two weeks´ exposure to hypoxia with a significant increase in mean pulmonary arterial pressure (MPAP), however, the increase was much less pronounced in the former. The attenuation of hypoxic pulmonary hypertension in TGR as compared to HanSD rats was associated with inhibition of ACE gene expression and activity, inhibition of AT₁receptor gene expression and suppression of ANG II levels in lung tissue. Simultaneously, there was an increase in lung ACE2 gene expression and activity and, in particular, ANG 1-7 concentrations and Mas receptor gene expression. We propose that a combination of suppression of ACE/ANG II/AT₁receptor axis and activation of ACE2/ANG 1-7/Mas receptor axis of the RAS in the lung tissue is the main mechanism explaining attenuation of hypoxic pulmonary hypertension in TGR as compared with HanSD rats.

References provided by Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc15040038
003      
CZ-PrNML
005      
20190920125028.0
007      
ta
008      
151230s2015 xr ad f 000 0|eng||
009      
AR
024    7_
$a 10.33549/physiolres.932861 $2 doi
035    __
$a (PubMed)25194138
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xr
100    1_
$a Hampl, Václav, $u Department of Physiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic $d 1962- $7 nlk20030127352
245    10
$a Intrapulmonary activation of the angiotensin-converting enzyme type 2/angiotensin 1-7/G-protein-coupled Mas receptor axis attenuates pulmonary hypertension in Ren-2 transgenic rats exposed to chronic hypoxia / $c V. Hampl, J. Herget, J. Bíbová, A. Baňasová, Z. Husková, Z. Vaňourková, Š. Jíchová, P. Kujal, Z. Vernerová, J. Sadowski, L. Červenka
520    9_
$a The present study was performed to evaluate the role of intrapulmonary activity of the two axes of the renin-angiotensin system (RAS): vasoconstrictor angiotensin-converting enzyme (ACE)/angiotensin II (ANG II)/ANG II type 1 receptor (AT₁) axis, and vasodilator ACE type 2 (ACE2)/angiotensin 1-7 (ANG 1-7)/Mas receptor axis, in the development of hypoxic pulmonary hypertension in Ren-2 transgenic rats (TGR). Transgene-negative Hannover Sprague-Dawley (HanSD) rats served as controls. Both TGR and HanSD rats responded to two weeks´ exposure to hypoxia with a significant increase in mean pulmonary arterial pressure (MPAP), however, the increase was much less pronounced in the former. The attenuation of hypoxic pulmonary hypertension in TGR as compared to HanSD rats was associated with inhibition of ACE gene expression and activity, inhibition of AT₁receptor gene expression and suppression of ANG II levels in lung tissue. Simultaneously, there was an increase in lung ACE2 gene expression and activity and, in particular, ANG 1-7 concentrations and Mas receptor gene expression. We propose that a combination of suppression of ACE/ANG II/AT₁receptor axis and activation of ACE2/ANG 1-7/Mas receptor axis of the RAS in the lung tissue is the main mechanism explaining attenuation of hypoxic pulmonary hypertension in TGR as compared with HanSD rats.
650    _2
$a angiotensin I $x metabolismus $7 D000803
650    _2
$a angiotensin II $x metabolismus $7 D000804
650    _2
$a zvířata $7 D000818
650    _2
$a hypoxie $x komplikace $x enzymologie $x patofyziologie $7 D000860
650    _2
$a arteriální tlak $7 D062186
650    _2
$a modely nemocí na zvířatech $7 D004195
650    _2
$a plicní hypertenze $x enzymologie $x genetika $x patofyziologie $x prevence a kontrola $7 D006976
650    _2
$a plíce $x enzymologie $7 D008168
650    _2
$a peptidové fragmenty $x metabolismus $7 D010446
650    _2
$a angiotensin konvertující enzym $x metabolismus $7 D007703
650    _2
$a protoonkogenní proteiny $x metabolismus $7 D011518
650    _2
$a potkani Sprague-Dawley $7 D017207
650    _2
$a potkani transgenní $7 D055647
650    _2
$a receptor angiotensinu typ 1 $x metabolismus $7 D044140
650    _2
$a receptory spřažené s G-proteiny $x metabolismus $7 D043562
650    _2
$a renin $x genetika $x metabolismus $7 D012083
650    12
$a renin-angiotensin systém $7 D012084
650    _2
$a signální transdukce $7 D015398
650    _2
$a vazokonstrikce $7 D014661
650    _2
$a vazodilatace $7 D014664
655    _2
$a časopisecké články $7 D016428
655    _2
$a práce podpořená grantem $7 D013485
700    1_
$a Herget, Jan, $d 1945-2019 $7 nlk19990073223 $u Department of Physiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic
700    1_
$a Bíbová, Jana, $d 1971- $7 xx0037207 $u Department of Physiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic
700    1_
$a Baňasová, Alena, $d 1973- $7 xx0074189 $u Department of Pathophysiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic
700    1_
$a Husková, Zuzana, $d 1978- $7 xx0074206 $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
700    1_
$a Vaňourková, Zdeňka, $d 1973- $7 xx0074217
700    1_
$a Jíchová, Šárka. $7 xx0239935 $u Department of Physiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic; Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
700    1_
$a Kujal, Petr $7 xx0244311 $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic; Department of Pathology, Third Faculty of Medicine, Charles University, Prague, Czech Republic
700    1_
$a Vernerová, Zdenka, $d 1960-2020 $7 jo2002104672 $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic; Department of Pathology, Third Faculty of Medicine, Charles University, Prague, Czech Republic
700    1_
$a Sadowski, Janusz, $d 1937- $7 xx0227641 $u Department of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Science, Warsaw, Poland
700    1_
$a Červenka, Luděk, $d 1967- $7 xx0037105 $u Department of Pathophysiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic; Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
773    0_
$w MED00003824 $t Physiological research $x 1802-9973 $g Roč. 64, č. 1 (2015), s. 25-38
856    41
$u http://www.biomed.cas.cz/physiolres/ $y domovská stránka časopisu
910    __
$a ABA008 $b A 4120 $c 266 $y 4 $z 0
990    __
$a 20151230 $b ABA008
991    __
$a 20190920125420 $b ABA008
999    __
$a ok $b bmc $g 1103706 $s 923265
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2015 $b 64 $c 1 $d 25-38 $e 20140905 $i 1802-9973 $m Physiological research $n Physiol. Res. (Print) $x MED00003824
GRA    __
$a NT14085 $p MZ0
GRA    __
$a NT13358 $p MZ0
LZP    __
$b NLK118 $a Pubmed-20151230

Find record

Citation metrics

Archiving options