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

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WU Yaqiong TAKAHASHI Hidenori SUZUKI Etsu KRUŽLIAK Peter SOUČEK Miroslav UEHARA Yoshio

Rok publikování 2016
Druh Článek v odborném periodiku
Časopis / Zdroj Hypertension Research
Fakulta / Pracoviště MU

Lékařská fakulta

Citace
Doi http://dx.doi.org/10.1038/hr.2015.132
Obor Ostatní lékařské obory
Klíčová slova angiotensin; Dahl rat; kidney damage; RGS2; salt hypertension
Popis 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.

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