Cell proliferation and morphometric changes in the rat kidney during postnatal development

Márquez, Marı́a Gabriela; Cabrera, Isabel; Serrano, Diego; Sterín-Speziale, Norma

doi:10.1007/s00429-002-0262-9

Cited by 61 publications

(71 citation statements)

References 15 publications

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“…21,36 Corroborating previous findings, 27,28 the present study demonstrated that, although the overall, pressor, and depressor slopes of the acute RAP-RIHP relationship are not different between strains, there is a rightward shift toward a greater RAP in 4-week-old SHRs relative to WKY rats. This finding not only supports the proposed cascade of players in pressurenatriuresis (ie, medullary blood flow, RIHP, urine flow, and sodium excretion) 37 but also, more importantly, the hypothesis that renal medullary vascular resistance properties are elevated in young SHRs 28,34 after completion of postnatal renal organogenesis (ie, postnatal day 30). 28,34 This notion is further supported by the moment-to-moment nature of RIHP responses (ie, Ͻ2 s) to changes in RAP in 4-week-old rats.…”

Section: Discussionsupporting

confidence: 74%

“…This finding not only supports the proposed cascade of players in pressurenatriuresis (ie, medullary blood flow, RIHP, urine flow, and sodium excretion) 37 but also, more importantly, the hypothesis that renal medullary vascular resistance properties are elevated in young SHRs 28,34 after completion of postnatal renal organogenesis (ie, postnatal day 30). 28,34 This notion is further supported by the moment-to-moment nature of RIHP responses (ie, Ͻ2 s) to changes in RAP in 4-week-old rats. Specifically, it appears that there is an underlying vascular basis for this component of the pressure-natriuresis mechanism, because it is unlikely that slower-acting neurohumoral mechanisms play a role in altering the acute functioning of this relationship.…”

Section: Discussionsupporting

confidence: 74%

“…[31][32][33] However, it remains unknown whether increases in renal medullary vascular resistance properties, and thereby pressure-natriuresis, occur in weaning SHRs (ie, 4 weeks old), at a time when renal organogenesis is complete. 34 We hypothesized that young SHRs are programmed to have increased vascular resistance properties and a rightward shift in the acute pressure-natriuresis mechanism before elevations in arterial pressure. Thus, the objective of the present study was to assess vascular resistance properties and the moment-to-moment RAP-RIHP relationship in weightmatched SHRs and WKY rats at 2 and/or 4 weeks of age.…”

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confidence: 99%

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Altered Vascular Resistance Properties and Acute Pressure-Natriuresis Mechanism in Neonatal and Weaning Spontaneously Hypertensive Rats

2012

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Abstract-Although it has been extensively scrutinized, the factor(s) involved in the initiation and development of hypertension in spontaneously hypertensive rats (SHRs) remains unresolved. The objective of the present study was to determine whether, early in development, the causal mechanism(s) for the development of hypertension in young SHRs involves an integration of 2 processes, specifically an upregulation of structurally based vascular resistance properties and a rightward shift in the hemodynamic component of pressure-natriuresis. Mean arterial pressure was determined in conscious 4-week-old SHRs and Wistar-Kyoto rats via previously implanted aortic catheters. Structurally based hindlimb vascular resistance properties were assessed in 2-and 4-week-old SHRs and Wistar-Kyoto rats. Renal interstitial hydrostatic pressure was measured after short-term manipulations of renal arterial pressure (RAP) in 4-week-old, anesthetized rats. Although mean arterial pressure in conscious SHRs (113Ϯ5 mmHg) and Wistar-Kyoto rats (110Ϯ6 mmHg) was not significantly different at 4 weeks of age, SHRs at 2 and 4 weeks of age already had increases in structurally based vascular resistance properties of Ϸ30% above age-and weight-matched Wistar-Kyoto rats. Furthermore, the acute RAP-renal interstitial hydrostatic pressure relationship was found to be linear in both strains, and the temporal coupling of the stimulus to response was rapid; that is, renal interstitial hydrostatic pressure responses to changes in RAP were Ͻ2 s. Although the slope of the RAP-renal interstitial hydrostatic pressure relationship was not significantly different between strains, the relationship was significantly shifted (18%) to higher RAPs in SHRs. These results suggest that alterations in both vascular structure and renal function in young SHRs occur before elevations in mean arterial pressure. A lthough the factors responsible for the initiation and development of genetic hypertension have been extensively studied in the spontaneously hypertensive rat (SHR), the basis and time course for blood pressure elevation remain enigmatic. Specifically, what remains controversial is whether the 2 most widely studied processes, vascular abnormalities and renal dysfunction, lead to increases in arterial pressure or vice versa.Since the 1970s, 1 it has been well established that vascular abnormalities, such as increases in vascular resistance, vascular reactivity to vasoconstrictors, and media:lumen ratio, are associated with hypertension in the adult SHR.1-3 Despite the number of studies describing vascular morphometric and histological differences in young SHRs, 4-9 evidence linking blood pressure elevations with vascular structural and functional changes remains unresolved in the neonatal and weaning SHRs. The hypothesis that vascular structural changes antecede and initiate a rise in arterial pressure has been disputed for 2 main reasons, the presence 8,10-13 or lack 4-7,9,14,15 of blood pressure elevation in studies of young SHRs and substantial differences be...

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Section: Discussionsupporting

confidence: 74%

Section: Discussionsupporting

confidence: 74%

mentioning

confidence: 99%

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Altered Vascular Resistance Properties and Acute Pressure-Natriuresis Mechanism in Neonatal and Weaning Spontaneously Hypertensive Rats

2012

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“…The last nephron anlages to be formed develop into functional nephron by 10 days after birth. 14,15 Rats enter puberty at the age of 4 weeks and reach sexual maturity at 8 weeks. We used an in situ probe specific to the transgene as well as a probe that detected both the transgenic and endogenous Anks6 mRNA.…”

Section: Anks6mentioning

confidence: 99%

Transgenic Overexpression of Anks6 Causes Polycystic Kidney Disease in Rats

Neudecker

Walz

Menon

et al. 2010

The American Journal of Pathology

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The PKD/Mhm(cy/؉) rat is a widely used animal model for the study of human autosomal dominant polycystic kidney disease, one of the most common genetic disorders, affecting one in 1000 individuals. We identified a new gene, Anks6, which is mutated (Anks6 (p.R823W) ) in PKD/Mhm(cy/؉) rats. The evidence for a causal link between Anks6 (p.R823W) and cystogenesis is still lacking, and the function of Anks6 is presently unknown. This study presents a novel transgenic rat model that overexpresses the mutated 2.8-kb Anks6 (p.R823W) cDNA in the renal tubular epithelium. The transgenic Anks6 (p.R823W) acts in a dominant-negative fashion and causes a predictable polycystic phenotype that largely mimics the general characteristics of the PKD/Mhm(cy/؉) rats. Cyst development is accompanied by enhanced c-myc expression and continuous proliferation, apoptosis, and de-differentiation of the renal tubular epithelium as well as by a lack of translational up-regulation of p21 during aging. Using Northern blot analysis and in situ hybridization studies , we identified the first 10 days of age as the period during which transgene expression precedes and initiates cystic growth. Thus , we not only provide the first in vivo evidence for a causal link between the novel Anks6 (p.R823W) gene mutation and polycystic kidney disease , but we also developed a new transgenic rat model that will serve as an important resource for further exploration of the still unknown function

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“…9 We tracked the morphogenesis of the renal medulla into adult life. At 30 to 33 weeks of age, the renal papilla remained hypoplastic (Figures 3, A and B), but aquaporin 2 (AQP2) expression was normal in residual papillary collecting ducts (Supplemental Figure 2).…”

mentioning

confidence: 99%

Targeted Inactivation of EGF Receptor Inhibits Renal Collecting Duct Development and Function

Zhang¹,

Pascuet²,

Hueber³

et al. 2010

Journal of the American Society of Nephrology

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Cell proliferation and morphometric changes in the rat kidney during postnatal development

Cited by 61 publications

References 15 publications

Altered Vascular Resistance Properties and Acute Pressure-Natriuresis Mechanism in Neonatal and Weaning Spontaneously Hypertensive Rats

Altered Vascular Resistance Properties and Acute Pressure-Natriuresis Mechanism in Neonatal and Weaning Spontaneously Hypertensive Rats

Transgenic Overexpression of Anks6 Causes Polycystic Kidney Disease in Rats

Targeted Inactivation of EGF Receptor Inhibits Renal Collecting Duct Development and Function

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