Estudo da pressão arterial e manipulação renal de sodio em ratos diabeticos induzidos pela administração de estreptozocina : implicações do sistema nitroxidergico

AUTOR(ES)
DATA DE PUBLICAÇÃO

2001

RESUMO

The role ofthe kidney in the control ofhydrosaline homeostasis in patients or experimental models with diabetes mellitus has been striking demonstrated by several studies. Recently, growing evidence suggesting that precocious tubular dysfunction may precede glomerular modifications and influence directly the renal function and cardiovascular homeostase. However, no data are available that examine in details the sodium and potassium tubule handling changes at time-dependent fashion in models of streptozotocin-induced diabetes mellitus (DM). AIso, we hypothesized that a possible nitroxidergic contribution may modulate the renal function and consequently changing the urinary sodium excretion. To test this hypothesis, we investigated the effects of streptozotocin-induced diabetes mellitus on tubule sodium handling of unanesthetized, unrestrained rats and their controIs, by lithium c1earance. AIso, to examine the influence of nitroxidergic system inhibition on renal function rats were assigned randomly to one of four groups: (1) control rats, (2) streptozotocin-induced (STZ) DM rats, (3) L-NAME treated rats and (4) STZ-induced DM, L-NAME treated rats. In the current studies, we demonstrated that diabetic rats treated with streptozotocin showed a substantial and time-related increase in the urinary output of sodium (Control FENa + , first week: 0.I27:t0.009 %; forth week: 0.132 :t0.02 % and STZ induced DM FENa+ , first week: 0.244 :t0.05 %; forth week:0.529:t0.009 %) and potassium (Control FEK+ , first week: 0.085 :tO.OI %; forth week: 0.118:t0.03 % and STZ induced DM FEK+ , first week: 0.118:t0.Ol %; forth week:0.276:t0.02 %), and did not confirm the hypothesis that the renal ion excretion in STZ-induced DM, L-NAME treated rats is, at least in part, related to changes in NOS activity (L-NAME FENa+ , first week: 0.459 :t0.07 %; forth week: 1.190 :t0.25 % and STZ-induced DM L-NAME- treated FENa+ , first week: 0.732:tO.20 %; forth week: 1.797:t0.22 %). In addition, we showed that renal sodium handling changes occurred by increasing post-proximal tubule sodium rejection (FEPPNa+) despite an unchanged glomerular filtration rate (CCr) in the proportion ofthe sodium load filtered and arterial blood pressure. Thus, the observed increase in renal sodium and potassium excretion may be due to the inability of renal tubules to handle the electrolytes, with a promoted disruption in glomerotubular balance. Together, these fmdings may suggest that a possible precocious misleading of post-proximal tubular segment of nephron without any change of glomerular filtration rate or hemodynamic dysfunction in STZ-induced rats. Further studies are required to investigate and understand this tubular involvement in dysfunctional diabetes-tubular kidney interaction.

ASSUNTO(S)

oxido nitrico diabetes pressão arterial

ACESSO AO ARTIGO

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