2016
Impaired response of regulator of G alpha q signaling-2 mRNA to angiotensin II and hypertensive renal injury in Dahl salt-sensitive rats
WU, Yaqiong; Hidenori TAKAHASHI; Etsu SUZUKI; Peter KRUŽLIAK; Miroslav SOUČEK et al.Základní údaje
Originální název
Impaired response of regulator of G alpha q signaling-2 mRNA to angiotensin II and hypertensive renal injury in Dahl salt-sensitive rats
Autoři
WU, Yaqiong; Hidenori TAKAHASHI; Etsu SUZUKI; Peter KRUŽLIAK; Miroslav SOUČEK a Yoshio UEHARA
Vydání
Hypertension Research, London, Nature Publishing Group, 2016, 0916-9636
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
30000 3. Medical and Health Sciences
Stát vydavatele
Velká Británie a Severní Irsko
Utajení
není předmětem státního či obchodního tajemství
Impakt faktor
Impact factor: 3.581
Označené pro přenos do RIV
Ano
Kód RIV
RIV/00216224:14110/16:00089334
Organizační jednotka
Lékařská fakulta
UT WoS
EID Scopus
Klíčová slova anglicky
angiotensin; Dahl rat; kidney damage; RGS2; salt hypertension
Štítky
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 3. 8. 2016 15:41, Soňa Böhmová
Anotace
V originále
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 Gaq 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.