Low sodium chloride content in a multideficient diet induces renal vasodilatation in rats

Paixão, Ana D.O.; Nunes, F.lávia A.; Monteiro, Josélia C; Maciel, Cristiana Ramalho

doi:10.1016/s0271-5317(02)00494-3

Cited by 8 publications

(8 citation statements)

References 9 publications

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“…However, some malnourished litters of dams on this multideficient diet reached the body weight of the control group in adult life (Paixão et al 2001(Paixão et al , 2005. One explanation for this discrepancy is the variation in the content of sodium chloride in the multideficient diet prepared at different times before use (Paixão et al 2003). A low sodium intake during perinatal life jeopardizes growth Body weight at birth (g) 6.4 ± 0.1 (n = 30) 3.9 ± 0.1 * (n = 30) --Body weight at weaning (g) 68 ± 0.4 (n = 30) 55 ± 1.2 * (n = 30) --Body weight at 70 days of age (g) 308 ± 2 (n = 9) 278 ± 8 * (n = 10) 331 ± 7 (n = 9) 318 ± 9 † (n = 8) Kidney weight at 70 days of age (g)…”

Section: Discussionmentioning

confidence: 98%

“…However, some malnourished litters of dams on this multideficient diet reached the body weight of the control group in adult life (Paixão et al 2001, 2005). One explanation for this discrepancy is the variation in the content of sodium chloride in the multideficient diet prepared at different times before use (Paixão et al 2003). A low sodium intake during perinatal life jeopardizes growth in young rats (Ray et al 1992; Roy‐Clavel et al 1999; da Silva et al 2003).…”

Section: Discussionmentioning

confidence: 99%

“…Malnutrition was induced through a multideficient diet, as previously described (Teodósio et al 1990; Paixão et al 2001, 2003, 2005). The ingredients of the multideficient diet (g g −1 , expressed as a percentage) comprised beans (18.34), manioc flour (64.81), jerked meat (3.74) and sweet potato (12.76), which were cooked, dehydrated at 60°C and pulverized.…”

Section: Methodsmentioning

confidence: 99%

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Renal function in juvenile rats subjected to prenatal malnutrition and chronic salt overload

Magalhães¹,

Silveira

Mota

et al. 2006

Experimental Physiology

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Dietary sodium may contribute to hypertension and to cardiovascular and renal disease if a primary deficiency of the kidney to excrete sodium exists. In order to investigate whether chronic 1% NaCl in the drinking water changes blood pressure and renal haemodynamics in juvenile Wistar rats subjected to prenatal malnutrition, an evaluation of plasma volume, oxidative stress in the kidney, proteinuria and renal haemodynamics was carried out. Malnutrition was induced by a multideficient diet. Mean arterial pressure, renal blood flow and glomerular filtration rate (GFR) were measured using a blood pressure transducer, a flow probe and inulin clearance, respectively. Plasma volume and oxidative stress were measured by means of the Evans Blue method and by monitoring thiobarbituric acid reactive substances (TBARS) in the kidneys, respectively. Urinary protein was measured by precipitation with 3% sulphosalicylic acid. It was observed that prenatally malnourished rats presented higher values of plasma volume (26%, P < 0.05), kidney TBARS (43%, P < 0.01) and blood pressure (10%, P < 0.01) when compared with the control group. However, they showed no change in renal haemodynamics or proteinuria. Neither prenatally malnourished nor control rats treated with sodium overload presented plasma volume or blood pressure values different from their respective control groups, but both groups presented elevated proteinuria (P < 0.01). The prenatally malnourished group treated with sodium overload presented higher values of kidney TBARS, GFR and filtration fraction (58, 87 and 72% higher, respectively, P < 0.01) than its respective control group. In summary, sodium overload did not exacerbate the hypertension in juvenile prenatally malnourished rats, but induced renal haemodynamic adjustments compatible with the development of renal disease.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Renal function in juvenile rats subjected to prenatal malnutrition and chronic salt overload

Magalhães¹,

Silveira

Mota

et al. 2006

Experimental Physiology

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“…The standard diet contained (in g ⁄ g %): protein 23, carbohydrates 41, lipids 2.5, fibre 9 and minerals 8 (Na + 0.28), totaling 278 kcal (as indicated by the manufacturer, Purina Agribands). Even though some studies described hypertension in Northeastern Brazil associated with high dietary salt supplement in the diet [1], we decided to preserve the usual lower Na + content of the deficient diet that is widely used [23].…”

Section: Methodsmentioning

confidence: 99%

“…Renal haemodynamics were measured after anaesthesia with sodium pentobarbital (60 mg ⁄ kg BW, i.p. ), as previously described [23,25,27]. Briefly, animals (C, Maln, N-C and N-Maln groups) were tracheostomized and the left femoral artery, both jugular veins and the left ureter were catheterized.…”

Section: Methodsmentioning

confidence: 99%

Prenatal Undernutrition Changes Renovascular Responses of Nimesulide in Rat Kidneys

Silva

Veira-Filho

Barreto

et al. 2010

Basic Clin Pharma Tox

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Several studies in the Northeastern region of Brazil have demonstrated an association between hypertension in adult populations and prenatal and postnatal undernutrion. The central hypothesis we proposed was that hypertension could be favoured by programmed alterations in branches of the renal arachidonic pathway and consequently in counter-balancing the renin angiotensin system, especially during treatments with cyclooxygenase inhibitors. We assessed the influence of subchronic (21 days) and acute administration of nimesulide, a preferential cyclooxygenase-2 (COX-2) inhibitor, on mean blood pressure (MAP), renal blood flow (RBF), glomerular filtration rate (GFR) and urinary output (U v ) in adult rats that were prenatally undernourished. Undernutrition per se led to the onset of mild hypertension in adult offspring, whereas subchronic nimesulide treatment increased MAP in control and elicited further augmentation in undernourished animals. The drug (i) decreased RBF and GFR in controls by 50%, whereas no effect was detected in the undernourished group, and (ii) increased U v by 25% in controls, an effect that was potentiated by 200% in programmed animals. In contrast, acute nimesulide administration decreased U v , with the hypertensive effect of the drug being potentiated during dehydration. These findings demonstrate that prenatal nutritional programming differentially modulates adult renovascular responses to nimesulide in the cortex and medulla, which may exacerbate the deleterious effects of COX-2 inhibition in the kidney.Epidemiological studies indicate an association between undernutrition in early life and hypertension in adults in rural areas of Northeast Brazil [1]. Experimental undernutrition using a diet mimicking that widely used by human beings in these regions [2] leads to alterations in renal structure and function [3], including those related to angiotensin II-modulated renal fluid handling [4] that could be associated with the onset of hypertension in adulthood. Maternal dietary restriction using different protocols has demonstrated programming of renal lesions in cortex and medulla that could be involved in alterations of renovascular responses [5][6][7], although the role of the kidney in perinatal programming of long-term alterations of arterial blood pressure has had only minor attention until recently [8].Since the intrarenal renin ⁄ angiotensin II system might be modulated by arachidonic acid-derived vasoactive products reviewed in [9,10], we have postulated that programming of adult hypertension could also involve alterations in key steps of the renal arachidonic pathway, such as those mediated by cyclooxygenases. Consequently, the renovascular responses of adults become altered after undernourishment in early life. We also hypothesized that possible hidden alteration in the intrarenal arachidonic acid routes could be exacerbated during the treatment with cyclooxygenase inhibitors.The adult kidney is one of the few organs that constitutively produce cyclooxygenase-2 (COX-2), a...

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Reduced cholesterol levels in renal membranes of undernourished rats may account for urinary Na+ loss

et al. 2012

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Low sodium chloride content in a multideficient diet induces renal vasodilatation in rats

Cited by 8 publications

References 9 publications

Renal function in juvenile rats subjected to prenatal malnutrition and chronic salt overload

Renal function in juvenile rats subjected to prenatal malnutrition and chronic salt overload

Prenatal Undernutrition Changes Renovascular Responses of Nimesulide in Rat Kidneys

Reduced cholesterol levels in renal membranes of undernourished rats may account for urinary Na+ loss

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