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      Does a Nephron Deficit in Rats Predispose to Salt-Sensitive Hypertension?

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          Aim: This study tested the hypothesis that a nephron deficit predisposes rats to salt-sensitive hypertension in adulthood. Methods: Female Wistar-Kyoto rats were fed a low (9%) or a normal (20%) protein diet during pregnancy and lactation. Male, birth-weight-matched offspring were paired. One rat from each pair was perfusion fixed at 4 weeks of age and the other rat at 40 weeks of age. Kidneys were removed and nephron number and total renal filtration surface area (FSA) determined using unbiased stereological techniques. The rats that were allowed to grow to adulthood had tail-cuff systolic blood pressure and body weight determined twice weekly. Between 30 and 40 weeks of age, a normal or a high-salt diet was fed to the rats. Results: The offspring of rats fed the low-protein diet were significantly smaller at birth, and at 4 weeks of age they had a significant reduction in kidney volume, nephron number, and total renal FSA when compared to controls. Tail-cuff systolic blood pressure in the offspring from 4 to 29 weeks of age did not significantly differ between the two groups. Administration of a high-salt diet from 30 to 40 weeks of age led to a significant increase in blood pressure in both dietary treatment groups; however, it was not exacerbated in the rats exposed to the low-protein diet in utero. Conclusions: Maternal protein restriction in rats did not lead to salt-sensitive hypertension. Nephron endowment and FSA did not correlate with blood pressure in adulthood.

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          Most cited references 22

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          Glomerular number and size in relation to age, kidney weight, and body surface in normal man.

          The number and size of glomeruli in normal, mature human kidneys were estimated by a direct and unbiased stereological method, the fractionator. The number was 617,000 on average, and the mean size 6.0 M microns3. Both glomerular number and size showed significant negative correlation to age and significant positive correlation to kidney weight. Apparently, humans loose glomeruli with age. Body surface area correlated positively to kidney weight and total glomerular volume but not to number of glomeruli. Body surface area correlates significantly with metabolic rate (Robertson and Reid, Lancet, 1: 940-943, 1952). Thus, intraspecies adaptation of kidney filtration capacity to the metabolic demand is performed by changing the size of glomeruli, i.e., the number of glomeruli in individuals of a given species is independent of the metabolic rate.
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            Is blood pressure inversely related to birth weight? The strength of evidence from a systematic review of the literature.

            To assess the strength of evidence for an inverse relationship between blood pressure and birth weight. A systematic review of the published literature. Published studies describing the relationship between blood pressure and birth weight since 1956. More than 66,000 subjects aged 0-71 years. Thirty-four studies described the relationship of blood pressure with birth weight. The majority of the studies of children and adults showed that blood pressure fell with increasing birth weight. Studies of adolescents were inconsistent. In neonates there was a positive relationship between blood pressure and birth weight. The pattern with age was supported by the limited number of studies with repeated measures and was dependent neither on the method of analysis nor on work from a single academic group or country. Blood pressure is inversely related to birth weight in children and in adults. The positive results in neonates and the inconsistency in adolescence may be related to the unusual growth dynamics during these phases of growth. Further studies should concentrate on the mechanisms which underlie the relationship.
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              Maternal protein restriction suppresses the newborn renin-angiotensin system and programs adult hypertension in rats.

              Restriction of maternal protein intake during rat pregnancy produces offspring that are hypertensive in adulthood, but the mechanisms are not well understood. Our purpose was to determine whether this adult hypertension could be programmed during development by suppression of the fetal/newborn renin-angiotensin system (RAS) and a consequent reduction in nephron number. Pregnant rats were fed a normal protein (19%, NP) or low-protein (8.5%, LP) diet throughout gestation. Birth weight was reduced by 13% (p < 0.0005), and the kidney/body weight ratio was reduced in LP pups. Renal renin mRNA levels were significantly reduced in newborn LP pups; renal renin concentration and renin immunostaining were suppressed. Renal tissue angiotensin II levels were also suppressed in newborn LP (0.079 +/- 0.002 ng/mg, LP versus 0.146 +/- 0.016 ng/mg, NP, p < 0.01). Mean arterial pressure in conscious, chronically instrumented adult offspring (21 wk) was higher in LP (135 +/- 1 mm Hg, LP versus 126 +/- 1 mm Hg, NP, p < 0.00007), and GFR normalized to kidney weight was reduced in LP (p < 0.04). The number of glomeruli per kidney was lower in adult LP offspring (21,567 +/- 1,694, LP versus 28,917 +/- 2,342, NP, p < 0.03), and individual glomerular volume was higher (1.81 +/- 0.16 10(6) microm(3), LP versus 1.11 +/- 0.10 10(6) microm(3), NP, p < 0.005); the total volume of all glomeruli per kidney was not significantly different. Thus, perinatal protein restriction in the rat suppresses the newborn intrarenal RAS and leads to a reduced number of glomeruli, glomerular enlargement, and hypertension in the adult.

                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                September 2004
                08 September 2004
                : 27
                : 4
                : 239-247
                Department of Anatomy and Cell Biology, Monash University, Clayton, Vic., Australia
                79868 Kidney Blood Press Res 2004;27:239–247
                © 2004 S. Karger AG, Basel

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                Figures: 6, Tables: 3, References: 42, Pages: 9
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