Effect of sodium overload on renal function of offspring from diabetic mothers
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ORIGINAL ARTICLE
Effect of sodium overload on renal function of offspring from diabetic mothers Luigi Rocco & Frida Zaladek Gil & Thaís Maria da Fonseca Pletiskaitz & Maria de Fátima Cavanal & Guiomar Nascimento Gomes
Received: 28 November 2007 / Revised: 23 April 2008 / Accepted: 28 April 2008 / Published online: 24 June 2008 # IPNA 2008
Abstract The aim if this study was to evaluate the effect of sodium overload on blood pressure and renal function in the offspring of diabetic rat mothers. Diabetes was induced with a single dose of streptozotocin before mating. Experimental groups were control (C), offspring from diabetic mother (D), control with sodium chloride (NaCl) overload (CS), and offspring from diabetic mother submitted to NaCl overload (DS). After weaning, all groups received food ad libitum; groups C and D had water ad libitum, and CS and DS received NaCl 0.15 M as drinking water. Renal morphology and function were evaluated in 3-month-old rats. Glomerular area, macrophage infiltration, interlobular artery wall thickness, and renal vascular resistance were significantly increased in CS, D, and DS compared with C. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were decreased in CS and D compared with C. In DS, GFR and fractional filtration were increased, suggesting a state of hyperfiltration. Hypertension was observed in groups D, CS, and DS from 2 months on and was more severe in DS. Our data suggest that diabetes during intrauterine development and salt overload beginning at an early age can cause hypertension and renal injury. When these conditions were associated, morphological and functional changes were much more intense, suggesting acceleration in the process of kidney injury. Keywords Hypertension . Kidney injury . Salt overload . Diabetes mellitus . Renal morphology L. Rocco : F. Z. Gil : T. M. da Fonseca Pletiskaitz : M. de Fátima Cavanal : G. N. Gomes (*) Department of Physiology, Federal University of São Paulo, Rua Botucatu 862 - 5° andar, São Paulo - S.P. 04023–900, Brazil e-mail: [email protected]
Introduction In recent decades, much research has examined the relationship between fetal growth conditions and susceptibility to pathologies in adulthood [1–3]. Experimental and clinical studies have demonstrated that sustained exposure of the fetus to elevated concentrations of glucose increases the risk of intrauterine death, prematurity, perinatal mortality, and congenital malformations [4–6]. Increased risk for cardiovascular diseases and diabetes has been observed in the offspring of diabetic mothers at adulthood [7–9]. Previous studies from our laboratory have shown that maternal diabetes in rats promotes systemic hypertension and glomerular hypertrophy in the offspring, which contribute to the progression of renal disease [10–12]. In this experimental rat model, treatment with L-arginine reduced hypertension and prevented glomeruli hypertrophy [11]. Systemic arterial hypertension is a multifactorial disorder in which, among others, genes controlling renal sodium ha
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