Conditional knockout of collecting duct bradykinin B2 receptors exacerbates angiotensin II-induced hypertension during high salt intake

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023001%3A_____%2F16%3A00059588" target="_blank" >RIV/00023001:_____/16:00059588 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11130/16:10323754

Výsledek na webu

<a href="http://www.tandfonline.com/doi/abs/10.3109/10641963.2015.1047945?journalCode=iceh20" target="_blank" >http://www.tandfonline.com/doi/abs/10.3109/10641963.2015.1047945?journalCode=iceh20</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3109/10641963.2015.1047945" target="_blank" >10.3109/10641963.2015.1047945</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Conditional knockout of collecting duct bradykinin B2 receptors exacerbates angiotensin II-induced hypertension during high salt intake

Popis výsledku v původním jazyce

We elucidated the role of collecting duct kinin B2 receptor (B2R) in the development of salt-sensitivity and angiotensin II (ANG II)-induced hypertension. To this end, we used a Cre-Lox recombination strategy to generate mice lacking Bdkrb2 gene for B2R in the collecting duct (Hoxb7-Cretg/+:Bdkrb2flox/flox). In 3 groups of control (Bdkrb2flox/flox) and 3 groups of UBBdkrb2-/- mice, systolic blood pressure (SBP) responses to high salt intake (4 or 8% NaCl; HS) were monitored by radiotelemetry in comparison with standard salt diet (0.4% NaCl) prior to and during subcutaneous ANG II infusion (1000 ng/min/kg) via osmotic minipumps. High salt intakes alone for 2 weeks did not alter SBP in either strain. ANG II significantly increased SBP equally in control (121 +- 2 to 156 +- 3 mmHg) and UBBdkrb2-/- mice (120 +- 2 to 153 +- 2 mmHg). The development of ANG II-induced hypertension was exacerbated by 4%HS in both control (125 +- 3 to 164 +- 5 mmHg) and UBBdkrb2-/- mice (124 +- 2 to 162 +- 3 mmHg) during 2 weeks. Interestingly, 8%HS caused a more profound and earlier ANG II-induced hypertension in UBBdkrb2-/- (129 +- 2 to 166 +- 3 mmHg) as compared to control (128 +- 2 to 158 +- 2 mmHg) and it was accompanied by body weight loss and increased mortality. In conclusion, targeted inactivation of B2R in the renal collecting duct does not cause salt-sensitivity; however, collecting duct B2R attenuates the hypertensive actions of ANG II under conditions of very high salt intake.

Název v anglickém jazyce

Conditional knockout of collecting duct bradykinin B2 receptors exacerbates angiotensin II-induced hypertension during high salt intake

Popis výsledku anglicky

We elucidated the role of collecting duct kinin B2 receptor (B2R) in the development of salt-sensitivity and angiotensin II (ANG II)-induced hypertension. To this end, we used a Cre-Lox recombination strategy to generate mice lacking Bdkrb2 gene for B2R in the collecting duct (Hoxb7-Cretg/+:Bdkrb2flox/flox). In 3 groups of control (Bdkrb2flox/flox) and 3 groups of UBBdkrb2-/- mice, systolic blood pressure (SBP) responses to high salt intake (4 or 8% NaCl; HS) were monitored by radiotelemetry in comparison with standard salt diet (0.4% NaCl) prior to and during subcutaneous ANG II infusion (1000 ng/min/kg) via osmotic minipumps. High salt intakes alone for 2 weeks did not alter SBP in either strain. ANG II significantly increased SBP equally in control (121 +- 2 to 156 +- 3 mmHg) and UBBdkrb2-/- mice (120 +- 2 to 153 +- 2 mmHg). The development of ANG II-induced hypertension was exacerbated by 4%HS in both control (125 +- 3 to 164 +- 5 mmHg) and UBBdkrb2-/- mice (124 +- 2 to 162 +- 3 mmHg) during 2 weeks. Interestingly, 8%HS caused a more profound and earlier ANG II-induced hypertension in UBBdkrb2-/- (129 +- 2 to 166 +- 3 mmHg) as compared to control (128 +- 2 to 158 +- 2 mmHg) and it was accompanied by body weight loss and increased mortality. In conclusion, targeted inactivation of B2R in the renal collecting duct does not cause salt-sensitivity; however, collecting duct B2R attenuates the hypertensive actions of ANG II under conditions of very high salt intake.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FA - Kardiovaskulární nemoci včetně kardiochirurgie

OECD FORD obor

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Projekt

<a href="/cs/project/NT14011" target="_blank" >NT14011: Vliv genové inaktivace B2 receptorů pro bradykinin v distálním tubulu myši na transport sodíku u experimentálních modelů hypertenze</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2016

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Clinical and experimental hypertension

ISSN

1064-1963

e-ISSN

—

Svazek periodika

38

Číslo periodika v rámci svazku

1

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

9

Strana od-do

1-9

Kód UT WoS článku

000367921300001

EID výsledku v databázi Scopus

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