Abstract

FELLET, Andrea et al. Aquaporin-2 Abundance Modulation in the Kidney of the Rat: The Effect of Nitric Oxide During the Hypovolemic State. Rev. argent. cardiol. [online]. 2008, vol.76, n.1, pp.35-41. ISSN 1850-3748.

We have previously demonstrated that hemorrhagic shock induces a time-dependent increase in the activity of nitric oxide synthase specific isoform. Such activation might be involved in modulation of cardiovascular function. It seems that the inhibition of the nitric oxide system prevents hemorrhage- induced heart rate changes seen in late stages of hypovolemic shock. The objective of this study was to assess if the inhibition of the nitric oxide system alters aquaporin-2 expression and/or location in the collecting-duct systems in kidneys of bleeding rats. Male Sprague-Dawley rats were used, divided in four groups (n = 15 for each group): a) normotensive rats (group N), b) hypovolemic rats (animals subjected to a 20% loss of the total volemia) (group H), c) normotensive rats pretreated with the nitric oxide synthase inhibitor N^G-nitro-L-arginine- methyl ester (group L-NAME N), and d) hypovolemic rats pretreated with the inhibitor (group L-NAME H). The distribution and the expression of aquaporin-2 were assessed 120 minutes after bleeding by immunohystochemical and Western blot analysis. An increase in aquaporin-2 expression was seen 120 after blood loss. Immunolocation showed aquaporin-2 inside the cytoplasm of collecting-duct main cells in kidneys of bleeding rats. Nitric oxide inhibition increased aquaporin-2 levels, especially in the apical membrane. Thus, the nitric oxide system might be associated with a progressive decrease in the expression of aquaporin-2 which may alter urine concentration as a response to hemorrhagic shock.

Keywords : Hemorrhage; Nitric Oxide; Aquaporins; Water Balance.

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