PMID- 31178756
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 1664-042X (Print)
IS  - 1664-042X (Electronic)
IS  - 1664-042X (Linking)
VI  - 10
DP  - 2019
TI  - The Effects of Bradykinin B1 Receptor Antagonism on the Myocardial and Vascular 
      Consequences of Hypertension in SHR Rats.
PG  - 624
LID - 10.3389/fphys.2019.00624 [doi]
LID - 624
AB  - It is known that non-steroidal anti-inflammatory drugs increase cardiovascular 
      (CV) morbidity and mortality. In this study, we examined whether a novel 
      anti-inflammatory drug, bradykinin B1 receptor antagonist (FGY-1153) treatment 
      could influence the development of hypertensive organ damages in spontaneously 
      hypertensive rats (SHR). SHRs were treated with low (FGY-120) or high dose 
      FGY-1153 (FGY-400) and with placebo (Control) for 26 weeks. Wistar-Kyoto rats 
      were used as aged-matched, normotensive controls (WKY). Body weight, food 
      consumption and blood pressure were measured regularly. Echocardiography was 
      performed at the beginning and at the end of the study. Light and electron 
      microscopic analysis of heart and great vessels were performed, and the extent of 
      fibrotic areas was measured. The phosphorylation state of prosurvival 
      Akt-1/glycogen synthase kinase (GSK)-3beta pathway and the activation of signaling 
      factors playing part in the fibrotic processes - mitogen activated protein 
      kinases (MAPKs), and TGF-beta/Smad2 - were monitored using Western-blot. Body weight 
      and food consumption as well as the elevated blood pressure in SHRs was not 
      influenced by FGY-1153 treatment. However, both doses of FGY-1153 treatment 
      decreased left ventricular (LV) hypertrophy and diastolic dysfunction in 
      hypertensive animals. Moreover systolic LV function was also preserved in FGY-120 
      group. Increased intima-media thickness and interstitial fibrosis were not 
      significantly diminished in great vessels. FGY-1153 treatment inhibited the 
      expression of TGFbeta and the phosphorylation of SMAD2 in the heart. Our results 
      suggest that the tested novel anti-inflammatory compound has no deleterious 
      effect on CV system, moreover it exerts moderate protective effect against the 
      development of hypertensive cardiopathy.
FAU - Deres, Laszlo
AU  - Deres L
AD  - Medical School, University of Pecs, Pecs, Hungary.
AD  - Szentagothai Research Centre, University of Pecs, Pecs, Hungary.
FAU - Eros, Krisztian
AU  - Eros K
AD  - Medical School, University of Pecs, Pecs, Hungary.
AD  - Szentagothai Research Centre, University of Pecs, Pecs, Hungary.
FAU - Horvath, Orsolya
AU  - Horvath O
AD  - Medical School, University of Pecs, Pecs, Hungary.
AD  - Szentagothai Research Centre, University of Pecs, Pecs, Hungary.
FAU - Bencze, Noemi
AU  - Bencze N
AD  - Medical School, University of Pecs, Pecs, Hungary.
AD  - Szentagothai Research Centre, University of Pecs, Pecs, Hungary.
FAU - Cseko, Csongor
AU  - Cseko C
AD  - Gedeon Richter Plc., Budapest, Hungary.
FAU - Farkas, Sandor
AU  - Farkas S
AD  - Gedeon Richter Plc., Budapest, Hungary.
FAU - Habon, Tamas
AU  - Habon T
AD  - 1st Department of Medicine, Clinical Centre, University of Pecs, Pecs, Hungary.
FAU - Toth, Kalman
AU  - Toth K
AD  - Szentagothai Research Centre, University of Pecs, Pecs, Hungary.
AD  - 1st Department of Medicine, Clinical Centre, University of Pecs, Pecs, Hungary.
FAU - Halmosi, Robert
AU  - Halmosi R
AD  - Szentagothai Research Centre, University of Pecs, Pecs, Hungary.
AD  - 1st Department of Medicine, Clinical Centre, University of Pecs, Pecs, Hungary.
LA  - eng
PT  - Journal Article
DEP - 20190521
PL  - Switzerland
TA  - Front Physiol
JT  - Frontiers in physiology
JID - 101549006
PMC - PMC6537226
OTO - NOTNLM
OT  - NSAIDs
OT  - bradykinin B1 receptor antagonism
OT  - cardiovascular remodeling
OT  - echocardiography
OT  - hypertensive target organ damages
OT  - spontaneously hypertensive rats
EDAT- 2019/06/11 06:00
MHDA- 2019/06/11 06:01
PMCR- 2019/05/21
CRDT- 2019/06/11 06:00
PHST- 2018/09/30 00:00 [received]
PHST- 2019/05/02 00:00 [accepted]
PHST- 2019/06/11 06:00 [entrez]
PHST- 2019/06/11 06:00 [pubmed]
PHST- 2019/06/11 06:01 [medline]
PHST- 2019/05/21 00:00 [pmc-release]
AID - 10.3389/fphys.2019.00624 [doi]
PST - epublish
SO  - Front Physiol. 2019 May 21;10:624. doi: 10.3389/fphys.2019.00624. eCollection 
      2019.