Sodium load combined with low doses of exogenous angiotensin II upregulate intrarenal angiotensin II.

The present study was designed to evaluate the effects of a salt load combined with exogenous low nonhypertensive angiotensin II (Ang II) doses on Ang II intrarenal regulation. Sprague-Dawley rats were infused with Ang II nonhypertensive doses (0.1 microg.kg(-1).h(-1) and 5 microg.kg(-1).h(-1)) and saline overload (Na 0.5 M, Na 1.0 M and Na 1.5 M) for 2 h (0.04 ml.min(-1)). Sodium tubular reabsorption, sodium urinary excretion and mean arterial pressure (MAP) were measured. Ang II was evaluated in the kidneys by immunohistochemistry. Ang II levels in glomeruli and vessels were exacerbated when sodium load and Ang II were given simultaneously, independently of MAP elevation. In tubules, Ang II staining in the presence of sodium overload was greater in the Ang 0.1 groups than in the Ang 5 groups. Compared with the controls, sodium tubular reabsorption rose in the Ang 0.1-Na 0.5 and Ang 0.1-Na 1 groups and sodium urinary excretion decreased in the Ang 5-Na 0.5 and Ang 5-Na 1 groups. MAP increased in the Ang 5-Na 1 and Ang 5-Na 1.5 groups. We conclude that local renal Ang II levels were upregulated when acute sodium overload and nonhypertensive Ang II doses were administered simultaneously in normal rats, independently from blood pressure and glomerular function changes.

Rosón MI ，Cao G ，Della Penna S ，Gorzalczany S ，Pandolfo M ，Medici C ，Fernández BE ，Toblli JE ... -  《-》

Angiotensin II increases intrarenal transforming growth factor-beta1 in rats submitted to sodium overload independently of blood pressure.

Rosón MI ，Cao G ，Della Penna S ，Gorzalczany S ，Pandolfo M ，Toblli JE ，Fernández BE ... -  《HYPERTENSION RESEARCH》

Different protective actions of losartan and tempol on the renal inflammatory response to acute sodium overload.

The aim of this work was to study the role of local intrarenal angiotensin II (Ang II) and the oxidative stress in the up-regulation of pro-inflammatory cytokines expression observed in rats submitted to an acute sodium overload. Sprague-Dawley rats were infused for 2 h with isotonic saline solution (Control group) and with hypertonic saline solution alone (Na group), plus the AT1 receptor antagonist losartan (10 mg kg(-1) in bolus) (Na-Los group), or plus the superoxide dismutase mimetic tempol (0.5 mg min(-1) kg(-1)) (Na-Temp group). Mean arterial pressure, glomerular filtration rate, and fractional sodium excretion (FE(Na)) were measured. Ang II, NF-kappaB, hypoxia inducible factor-1 alpha (HIF-1 alpha), transforming growth factor beta1 (TGF-beta1), smooth muscle actin (alpha-SMA), endothelial nitric oxide synthase (eNOS), and RANTES renal expression was evaluated by immunohistochemistry. Ang II, NF-kappaB, and TGF-beta1 and RANTES early inflammatory markers were overexpressed in Na group, accompanied by enhanced HIF-1 alpha immunostaining, lower eNOS expression, and unmodified alpha-SMA. Losartan and tempol increased FE(Na) in sodium overload group. Although losartan reduced Ang II and NF-kappaB staining and increased eNOS expression, it did not restore HIF-1 alpha expression and did not prevent inflammation. Conversely, tempol increased eNOS and natriuresis, restored HIF-1 alpha expression, and prevented inflammation. Early inflammatory markers observed in rats with acute sodium overload is associated with the imbalance between HIF-1 alpha and eNOS expression. While both losartan and tempol increased natriuresis and eNOS expression, only tempol was effective in restoring HIF-1 alpha expression and down-regulating TGF-beta1 and RANTES expression. The protective role of tempol, but not of losartan, in the inflammatory response may be associated with its greater antioxidant effects.

Rosón MI ，Della Penna SL ，Cao G ，Gorzalczany S ，Pandolfo M ，Toblli JE ，Fernández BE ... -  《-》

Renal interstitial hydrostatic pressure and natriuretic response to high doses of angiotensin II in pregnant rats.

Yu T ，Khraibi AA 《AMERICAN JOURNAL OF HYPERTENSION》

Angiotensin II natriuresis and anti-natriuresis: role of renal artery pressure in anaesthetized dogs.

Olsen ME ，Hall JE ，Montaini JP ，Guyton AC ... -  《-》