Impaired response of regulator of Gαq signaling-2 mRNA to angiotensin II and hypertensive renal injury in Dahl salt-sensitive rats

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F16%3A00063778" target="_blank" >RIV/00159816:_____/16:00063778 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1038/hr.2015.132" target="_blank" >http://dx.doi.org/10.1038/hr.2015.132</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1038/hr.2015.132" target="_blank" >10.1038/hr.2015.132</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Impaired response of regulator of Gαq signaling-2 mRNA to angiotensin II and hypertensive renal injury in Dahl salt-sensitive rats

Popis výsledku v původním jazyce

Dahl salt-sensitive (Dahl S) rats are prone to salt-dependent hypertension with severe organ damage, including stroke, cardiac failure and renal insufficiency. The mechanism for this susceptibility to kidney injury has not been elucidated. The present study proposed that an upregulation of intracellular signaling of angiotensin II (Ang-II) is responsible for the susceptibility to hypertensive kidney injury in Dahl S rats. Spontaneously hypertensive rats exhibited higher systolic blood pressure (SBP) and lower kidney damage than Dahl S rats fed a high-salt diet for 2 weeks. Ang-II infusion for 4 weeks significantly increased SBP in Dahl S and Dahl salt-resistant (Dahl R) rats fed a low-salt diet. The increase in SBP in Dahl S rats was associated with significant kidney injury with greater glomerular sclerosis (Po0.001). The expression of regulatory protein of Gαq signaling-2 (RGS2) mRNA in the aortic walls in response to Ang-II infusion was lower in Dahl S than Dahl R rats (Po0.05). Ang-II significantly increased RGS2 mRNA in the aorta in Dahl R rats, but the response was apparently blunted in Dahl S rats. These results suggest that Dahl S rats exhibit a blunted RGS2 response to Ang-II, and this blunted response may be partially responsible for the susceptibility to renal injury in Dahl S rats.

Název v anglickém jazyce

Impaired response of regulator of Gαq signaling-2 mRNA to angiotensin II and hypertensive renal injury in Dahl salt-sensitive rats

Popis výsledku anglicky

Dahl salt-sensitive (Dahl S) rats are prone to salt-dependent hypertension with severe organ damage, including stroke, cardiac failure and renal insufficiency. The mechanism for this susceptibility to kidney injury has not been elucidated. The present study proposed that an upregulation of intracellular signaling of angiotensin II (Ang-II) is responsible for the susceptibility to hypertensive kidney injury in Dahl S rats. Spontaneously hypertensive rats exhibited higher systolic blood pressure (SBP) and lower kidney damage than Dahl S rats fed a high-salt diet for 2 weeks. Ang-II infusion for 4 weeks significantly increased SBP in Dahl S and Dahl salt-resistant (Dahl R) rats fed a low-salt diet. The increase in SBP in Dahl S rats was associated with significant kidney injury with greater glomerular sclerosis (Po0.001). The expression of regulatory protein of Gαq signaling-2 (RGS2) mRNA in the aortic walls in response to Ang-II infusion was lower in Dahl S than Dahl R rats (Po0.05). Ang-II significantly increased RGS2 mRNA in the aorta in Dahl R rats, but the response was apparently blunted in Dahl S rats. These results suggest that Dahl S rats exhibit a blunted RGS2 response to Ang-II, and this blunted response may be partially responsible for the susceptibility to renal injury in Dahl S rats.

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/ED1.100%2F02%2F0123" target="_blank" >ED1.100/02/0123: Fakultní nemocnice u sv. Anny v Brně - Mezinárodní centrum klinického výzkumu (FNUSA - ICRC)</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2016

Kód důvěrnosti údajů

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

Název periodika

Hypertension Research

ISSN

0916-9636

e-ISSN

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Svazek periodika

39

Číslo periodika v rámci svazku

4

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

7

Strana od-do

210-216

Kód UT WoS článku

000373847300007

EID výsledku v databázi Scopus

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