-
Something wrong with this record ?
Endothelin A receptor blockade improves endothelium-dependent relaxation in obese woman
K. Gradin, B. Persson
Language English Country Czech Republic
Document type Journal Article
NLK
Directory of Open Access Journals
from 1991
Free Medical Journals
from 1998
ProQuest Central
from 2005-01-01
Medline Complete (EBSCOhost)
from 2006-01-01
Nursing & Allied Health Database (ProQuest)
from 2005-01-01
Health & Medicine (ProQuest)
from 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
from 1998
- MeSH
- Endothelin A Receptor Antagonists pharmacology therapeutic use MeSH
- Endothelium, Vascular drug effects metabolism MeSH
- Peptides, Cyclic pharmacology therapeutic use MeSH
- Hypertension drug therapy metabolism surgery MeSH
- Middle Aged MeSH
- Humans MeSH
- Obesity drug therapy metabolism surgery MeSH
- Organ Culture Techniques MeSH
- Receptor, Endothelin A physiology MeSH
- Adipose Tissue blood supply drug effects metabolism MeSH
- Vasodilation drug effects physiology MeSH
- Dose-Response Relationship, Drug MeSH
- Gastric Bypass trends MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
Hypertension in obesity is associated with increased insulin resistance, vascular mass and body mass index (BMI). The purpose of the study was to visualize endothelin-1 (ET-1) mediated constriction in arteries isolated from subcutaneous adipose tissue from obese hypertensive women previously operated by gastric bypass. Functional studies were conducted in a microvascular myograph. Expressed as percentage of contraction elicited by 124 mM KCl concentration-response curves for ET-1 were shifted leftward in arteries from obese hypertensive patients compared to healthy normotensive subjects. The vasodilator response to the ET-1 antagonist BQ123 (1 microM) was significantly higher in arteries from obese hypertensive patients (p<0.001). BQ123 induced relaxation was inhibited by NO synthase inhibitor L-NAME (0.1 nM). Preincubation with BQ123 enhanced the relaxation induced by acetylcholine (ACh; 0.1 nM - 0.1 mM) (p<0.001), but not that induced by NO donor sodium nitroprusside (SNP; 0.1 nM - 0.1 mM), in arteries from obese hypertensive patients. The present study show that hypertension yet prevail after gastric bypass surgery and the ET(A) receptor antagonist BQ123 may be a useful tool in reducing blood pressure in obese hypertensive patients.
Department of Pharmacology University of Gothenburg Sahlgrenska Academy Gothenburg Sweden
Division of Internal Medicine Sahlgrenska University Hospital Sahlgrenska Gothenburg Sweden
References provided by Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc19005329
- 003
- CZ-PrNML
- 005
- 20210531150957.0
- 007
- ta
- 008
- 190204s2018 xr d f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.33549/physiolres.933813 $2 doi
- 035 __
- $a (PubMed)29947537
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xr
- 100 1_
- $a Gradin, K. $u Department of Pharmacology, University of Gothenburg, Sahlgrenska Academy, Gothenburg, Sweden
- 245 10
- $a Endothelin A receptor blockade improves endothelium-dependent relaxation in obese woman / $c K. Gradin, B. Persson
- 520 9_
- $a Hypertension in obesity is associated with increased insulin resistance, vascular mass and body mass index (BMI). The purpose of the study was to visualize endothelin-1 (ET-1) mediated constriction in arteries isolated from subcutaneous adipose tissue from obese hypertensive women previously operated by gastric bypass. Functional studies were conducted in a microvascular myograph. Expressed as percentage of contraction elicited by 124 mM KCl concentration-response curves for ET-1 were shifted leftward in arteries from obese hypertensive patients compared to healthy normotensive subjects. The vasodilator response to the ET-1 antagonist BQ123 (1 microM) was significantly higher in arteries from obese hypertensive patients (p<0.001). BQ123 induced relaxation was inhibited by NO synthase inhibitor L-NAME (0.1 nM). Preincubation with BQ123 enhanced the relaxation induced by acetylcholine (ACh; 0.1 nM - 0.1 mM) (p<0.001), but not that induced by NO donor sodium nitroprusside (SNP; 0.1 nM - 0.1 mM), in arteries from obese hypertensive patients. The present study show that hypertension yet prevail after gastric bypass surgery and the ET(A) receptor antagonist BQ123 may be a useful tool in reducing blood pressure in obese hypertensive patients.
- 650 _2
- $a tuková tkáň $x krevní zásobení $x účinky léků $x metabolismus $7 D000273
- 650 _2
- $a vztah mezi dávkou a účinkem léčiva $7 D004305
- 650 _2
- $a antagonisté endotelinového receptoru A $x farmakologie $x terapeutické užití $7 D065130
- 650 _2
- $a cévní endotel $x účinky léků $x metabolismus $7 D004730
- 650 _2
- $a ženské pohlaví $7 D005260
- 650 _2
- $a žaludeční bypass $x trendy $7 D015390
- 650 _2
- $a lidé $7 D006801
- 650 _2
- $a hypertenze $x farmakoterapie $x metabolismus $x chirurgie $7 D006973
- 650 _2
- $a lidé středního věku $7 D008875
- 650 _2
- $a obezita $x farmakoterapie $x metabolismus $x chirurgie $7 D009765
- 650 _2
- $a orgánové kultury - kultivační techniky $7 D009924
- 650 _2
- $a cyklické peptidy $x farmakologie $x terapeutické užití $7 D010456
- 650 _2
- $a receptor endotelinu A $x fyziologie $7 D044022
- 650 _2
- $a vazodilatace $x účinky léků $x fyziologie $7 D014664
- 655 _2
- $a časopisecké články $7 D016428
- 700 1_
- $a Persson, B. $u Division of Internal Medicine, Sahlgrenska University Hospital, Sahlgrenska,Gothenburg, Sweden
- 773 0_
- $w MED00003824 $t Physiological research $x 1802-9973 $g Roč. 67, Suppl. 1 (2018), s. S167-S174
- 773 0_
- $t ET-15 $g (2018), s. S167-S174 $w MED00206979
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/29947537 $y Pubmed
- 910 __
- $a ABA008 $b A 4120 $c 266 $y 4 $z 0
- 990 __
- $a 20190204 $b ABA008
- 991 __
- $a 20210531150956 $b ABA008
- 999 __
- $a ok $b bmc $g 1376292 $s 1043534
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2018 $b 67 $c Suppl. 1 $d S167-S174 $i 1802-9973 $m Physiological research $n Physiol. Res. (Print) $x MED00003824
- BMC __
- $a 2018 $d S167-S174 $m ET-15 $x MED00206979
- LZP __
- $b NLK118 $a Pubmed-20190204