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Am J Physiol Renal Physiol (July 2, 2002). doi:10.1152/ajprenal.00322.2001
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Articles in PresS, published online ahead of print July 2, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00322.2001
Submitted on October 26, 2001
Accepted on June 28, 2002

Contribution of angiotensin II internalization to intrarenal angiotensin II levels in rats

Catherine Ingert1, Michele Grima2*, Catherine Coquard1, Mariette Barthelmebs1, and Jean-Louis Imbs2

1 Faculte de Medecine, Institut de Pharmacologie, Strasbourg, France
2 Faculte de Medecine, Institut de Pharmacologie, Strasbourg, France; Hopitaux universitaires de Strasbourg, Service d'Hypertension, des Maladies vasculaires et Pharmacologie clinique, Strasbourg, France

* To whom correspondence should be addressed. E-mail: michele.grima{at}pharmaco-ulp.u-strasbg.fr.

This study was designed to determine the involvement of AT1 receptors in the uptake of Angiotensin II (Ang II) in the kidney of rats exposed to different salt intake. Male Wistar-Kyoto rats were treated with a normal (NS: 1% NaCl, n=7) or a low salt diet (LS: 0.025% NaCl, n=7) combined (LS+LOS, n=7) or not (NS+LOS, n=7) with losartan (30 mg/kg/d), an AT1 receptor antagonist. Renin (RA) and Angiotensin converting enzyme (ACE) activities, Angiotensinogen (Aogen), Angiotensin I (Ang I) and Ang II levels were measured in plasma, renal cortex and medulla. In LS rats, in both plasma and renal cortex, the increase in RA was associated with an increase in Ang I and Ang II levels compared to NS rats, but intrarenal Ang II levels increased more than Ang I levels. In NS+LOS rats, the increase in RA in plasma was followed by a marked increase in plasma Ang I and Ang II levels compared to NS rats whereas in the kidney, the increase of renal RA was followed by a decrease of these peptides levels. The same pattern was observed in LS+LOS, but the decrease in renal Ang II levels was much more pronounced in LS+LOS rats than in NS+LOS rats. Our results suggest that the increase in renal Ang II levels following salt restriction results mainly from an uptake of Ang II, via AT1 receptors. Such elevated intrarenal Ang II levels could contribute to maintain sodium and fluid balance and arterial blood pressure during salt deficiency states.




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