Influence of renal nerves on renal function during development

Robillard, J; Guillery, Edward N.; Segar, Jeffrey L.; Merrill, David; José, Pedro A.

doi:10.1007/bf00852576

Cited by 15 publications

(11 citation statements)

References 22 publications

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“…Afferent renal innervation occurs early in fetal life, 34 and the renal nerves are suggested to play an important role in the proper development of the kidney. 35 Thus, in this model of reduced uterine perfusion, hypoxia may serve as a stimulus for increased renal afferent nerve activity, resulting in alterations during kidney development, leading to both structural and physiological changes linked to the increased risk for development of hypertension in the adult animal.…”

Section: Discussionmentioning

confidence: 99%

Renal Denervation Abolishes Hypertension in Low-Birth-Weight Offspring From Pregnant Rats With Reduced Uterine Perfusion

et al. 2005

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Abstract-Low birth weight is a risk factor for the subsequent development of hypertension in humans. We previously reported that reduced uterine perfusion in the pregnant rat results in growth-restricted offspring predisposed to the development of hypertension. The purpose of this study was to determine whether the sympathetic nervous system plays a role in mediating hypertension in this model of low birth weight. Key Words: hypertension, pregnancy Ⅲ rats Ⅲ renal nerves Ⅲ denervation Ⅲ sympathetic nervous system H ypertension is a multifactorial disorder thought to result from both genetic and environmental factor interactions. Recent epidemiological studies 1,2 suggest that a predisposition for development of hypertension may be programmed by factors initiated in utero, 3 an observation supported by many animal studies. 4 -7 Fetal malnutrition limits fetal growth and results in small-for-gestational-age newborns. 8,9 Findings from both epidemiological and animal studies suggest that fetal malnutrition may also program or permanently alter fetal structure and physiology, resulting in an increased risk for development of hypertension and cardiovascular disease. 3,10 -12 However, the mechanisms mediating low birth weight (LBW) and hypertension remain to be elucidated.In humans, few studies have examined the relationship between the sympathetic nervous system (SNS) and LBW, and controversy exists with regards to whether LBW individuals are associated with increases [13][14][15] or decreases in sympathetic activity. 16 Evidence for alterations in the SNS is noted in some animal models of intrauterine growth restriction (IUGR), because plasma levels of circulating catecholamines are increased. [17][18][19][20][21] This observation has been noted in growth-restricted offspring from pregnant rats fed a proteinrestricted diet during gestation, 17 in a naturally occurring model of IUGR using piglets, 18,19 and in a model of IUGR induced by placental insufficiency in the rat 20 and in sheep. 21 Additionally, hypoxia during fetal development leads to increased sympathetic innervation. 22,23 However, no further assessment of the SNS in association with IUGR has been examined.Nutrient and oxygen supply limitations are the components of the intrauterine environment that limit fetal growth and result in small-for-gestational-age newborns. Because IUGR within the Western world is more likely the result of reduced uterine perfusion, 24 we have developed a model of fetal programming induced by placental insufficiency caused by hypoxia and fetal undernutrition. 25 Using this model, we previously reported that reduced uterine perfusion initiated at day 14 of gestation in the rat results in growth-restricted offspring that are hypertensive as early as 4 weeks of age. 25 Furthermore, marked elevations in mean arterial pressure (MAP) remain evident in male growth-restricted offspring at 12 weeks of age. Because increased renal sympathetic nerve activity appears to be a causal mechanism in primary hypertension, 26 we determined the ro...

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Section: Discussionmentioning

confidence: 99%

Renal Denervation Abolishes Hypertension in Low-Birth-Weight Offspring From Pregnant Rats With Reduced Uterine Perfusion

et al. 2005

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“…The renal nerves not only influence renal hemodynamics and renin secretion but also seem to play an inductive role during renal ontogeny (Robillard et al 1993). In vitro studies have shown that the neural element may be involved in kidney differentiation (Sariola et al 1989).…”

Section: Discussionmentioning

confidence: 99%

“…Chemical sympathectomy affects normal renal development and function, confirming that sympathetic innervation exerts a major influence on both of them (Slotkin et al 1988a(Slotkin et al , 1988bGray et al 1991). Additional studies have shown that sympathetic renal nerves modulate renal hemodynamics in early gestation and fluid/electrolyte homeostasis in late gestation (Robillard et al 1993). Furthermore, renal nerves play an important role during the transition from fetal to newborn life (Smith et al 1991Page et al 1992).…”

Section: Introductionmentioning

confidence: 99%

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Ontogeny of intrinsic innervation in the human kidney

et al. 2004

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We aimed to define, for the first time, the ontogeny of intrarenal innervation and to assess the distribution and nature of parenchymal nerves in the human fetal kidney. Our material consisted of routinely-processed renal tissue sections from 17 human fetuses, six of 20-24 gestational weeks (gw) and 11 of 25-40 gw, and three adults. We used immunohistochemistry with antibodies to the pan-neural markers neuron-specific enolase (NSE), neurofilaments (NF), PGP9.5, S100, and the adrenergic marker tyrosine hydroxylase (TH). NSE-, NF-, S100-, and PGP9.5-positive nerves, associated with arterial and venous vasculature, were identified in the renal cortex from 20 gw onwards, and their density appeared to increase with gestation, reaching adult levels at 28 gw. Most of the intrarenal nerves were TH-positive. Nerve fibers extended from the corticomedullary region to the outer cortex, reaching the renal capsule in the 3rd trimester. In detail, NSE-, NF-, S100-, PGP9.5-, and TH-immunoreactive fibers were observed in close apposition to the renal artery and its branches, occasionally reaching the afferent and efferent arteriole (3rd trimester). Nerve fibers were detected in close apposition to the juxtaglomerular apparatus in the 2nd and 3rd trimesters. In the renal medulla, NSE-, PGP9.5-, S100-, and TH-positive nerve fibers were detected close to tubular cells as early as 20 gw. However, their density gradually decreased during the 3rd trimester, and they were not observed in the medulla of the adult kidney. In conclusion, the human fetal kidney appears richly innervated during the 2nd and 3rd trimesters. There is a progressive increase in the density of parenchymal nerve fibers towards term from the corticomedullary region to the cortex. Most intrarenal nerves are adrenergic and have a predominant perivascular distribution, implying that renal innervation plays an important functional role during intrauterine life.

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“…Specifically, alterations in peripheral sympathetic nervous control could result in impaired renal development, as evidence suggests that the renal nerves play an important role in renal development through stimulation of the renin-angiotensin system. 29,30 Thus, asymmetric growth restriction resulting from limited growth of selective organs in late gestation, owing to alterations in nutrient supply to rapidly developing organs, may result in improper development and subsequent hypertension.…”

Section: Organ Weights In a Rat Model Of Intrauterine Growth Restrictionmentioning

confidence: 99%

Placental Insufficiency Leads to Development of Hypertension in Growth-Restricted Offspring

2003

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Influence of renal nerves on renal function during development

Cited by 15 publications

References 22 publications

Renal Denervation Abolishes Hypertension in Low-Birth-Weight Offspring From Pregnant Rats With Reduced Uterine Perfusion

Renal Denervation Abolishes Hypertension in Low-Birth-Weight Offspring From Pregnant Rats With Reduced Uterine Perfusion

Ontogeny of intrinsic innervation in the human kidney

Placental Insufficiency Leads to Development of Hypertension in Growth-Restricted Offspring

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