Project description:Serum and glucocorticoid-induced kinase 1 (SGK1) activates the epithelial sodium channel (eNaC) in tubules. We examined renal SGK1 abundance in salt-adaptation and in salt-sensitive hypertension. Sprague-Dawley and Dahl salt-sensitive rats were placed on either 8% or 0.3% NaCl diets for 10 days. Plasma aldosterone levels were approximately 2.5-fold greater on 0.3% versus 8% NaCl diets in both rat strains. Both serum and glucocorticoid-induced kinase 1 transcript and protein abundance were less (P<0.01) in Sprague-Dawley rats and greater (P<0.01) in Dahl salt-sensitive rats on 8% versus 0.3% NaCl diets. The cDNA sequences of serum and glucocorticoid-induced kinase 1 in both strains of rat were the same. The present results provide evidence that the abundance of serum and glucocorticoid-induced kinase 1 in rat kidney may play a role in salt adaptation and the pathogenesis of hypertension and suggests that aldosterone is not the primary inducer of SGK1 in the Sprague-Dawley rat. Keywords = Rattus norvegicus, Sprague Dawley, Dahl SS/Jr, kidney, NaCl diet Keywords: other
Project description:Serum and glucocorticoid-induced kinase 1 (SGK1) activates the epithselial sodium channel (eNaC) in tubules. We examined renal SGK1 abundance in salt-adaptation and in salt-sensitive hypertension. Sprague-Dawley and Dahl salt-sensitive rats were placed on either 8% or 0.3% NaCl diets for 10 days. Plasma aldosterone levels were approximately 2.5-fold greater on 0.3% versus 8% NaCl diets in both rat strains. Both serum and glucocorticoid-induced kinase 1 transcript and protein abundance were less (P<0.01) in Sprague-Dawley rats and greater (P<0.01) in Dahl salt-sensitive rats on 8% versus 0.3% NaCl diets. The cDNA sequences of serum and glucocorticoid-induced kinase 1 in both strains of rat were the same. The present results provide evidence that the abundance of serum and glucocorticoid-induced kinase 1 in rat kidney may play a role in salt adaptation and the pathogenesis of hypertension and suggests that aldosterone is not the primary inducer of SGK1 in the Sprague-Dawley rat.
Project description:Dahl-Iwai (DI) salt-sensitive rats were studied using microarrays to identify gender-specific differences in the kidney, both basal differences and responses to a high salt diet. In DI rat kidneys, gene expression profiles demonstrated inflammatory and fibrotic responses selectively in females. Gonadectomy of DI rats abrogated gender differences in gene expression. Gonadectomized female and gonadectomized male DI rats both responded to high salt with the same spectrum of gene expression changes as intact female DI rats. Androgens dominated the gender selective responses to salt. Several androgen-responsive genes were identified with roles potentiating the differential responses to salt including increased male expression of Angiotensin-Vasopressin Receptor and Prolactin Receptor, decreased 5-alpha reductase, and mixed increases and decreases in expression of Cyp4a- genes that can produce eicosanoid hormones. These gender differences potentiate sodium retention by males, and increase kidney function during gestation by females. Keywords: Disease-State Analysis (Salt-Sensitive Hypertension)
Project description:Dahl-Iwai (DI) salt-sensitive rats were studied using microarrays to identify gender-specific differences in the kidney, both basal differences and responses to a high salt diet. In DI rat kidneys, gene expression profiles demonstrated inflammatory and fibrotic responses selectively in females. Gonadectomy of DI rats abrogated gender differences in gene expression. Gonadectomized female and gonadectomized male DI rats both responded to high salt with the same spectrum of gene expression changes as intact female DI rats. Androgens dominated the gender selective responses to salt. Several androgen-responsive genes were identified with roles potentiating the differential responses to salt including increased male expression of Angiotensin-Vasopressin Receptor and Prolactin Receptor, decreased 5-alpha reductase, and mixed increases and decreases in expression of Cyp4a- genes that can produce eicosanoid hormones. These gender differences potentiate sodium retention by males, and increase kidney function during gestation by females. Experiment Overall Design: - 68 samples/rats/data tables are represented. Experiment Overall Design: - One microarray was used for each sample. Experiment Overall Design: - 3 rat
Project description:To get more insight in cause and consequences of proteinuria, we studied glomerular gene expression patterns before and after the onset of increased urinary albumin excretion in a proteinuric rat strain. Spontaneously proteinuric Dahl salt-sensitive rats (Dahl SS) were compared to non-proteinuric, spontaneously hypertensive rats (SHR). In Dahl SS, UAE significantly increased starting from week 5 of age. Glomerular RNA profiles of 4- and 6 week-old rats were studied by Affymetrix microarrays. Keywords: Time course analysis
Project description:The objective of this study was to profile circular RNAs (circRNAs) in rat genetic models of cardiovascular and renal disease. Renal profiles were obtained from the Dahl Salt-Sensitive rat (S), the Dahl Salt-Resistant rat (R), the Spontaneously Hypertensive Rat (SHR) and the Wistar Kyoto rat (WKY).
Project description:We used Affymetrix GeneChips to expression profile kidneys from Dahl salt-senstive hypertensive inbred strain and less hypertensive S.LEW(D1MCO4x1x3Bx1) congenic strain to identify genes downstream of Adamts16 (the function of Adamts16 has yet to be fully delineated). The S.LEW(D1MCO4x1x3Bx1) congenic animal is an S rat containing the LEWIS allele for Adamts16 instead of the S allele. It is hypothesized that allelic differences in Adamts16 in inbred rats is responsible for blood pressure variance. We further hypothesize that gene expression differences in the kidneys of S.LEW(D1MCO4x1x3Bx1) versus S result from sequence differences between the S and LEWIS alleles of Adamts16. Lastly, the downstream genes differentially regulated by the Adamts16 alleles may provide insight pertaining to the mechanism of blood pressure differences. Gene expression differences resulting from these kidney comparisons will be compared to the gene expression profiling experiments comparing siRNA-mediated knockdown of Adamts16 in NRK-52E kidney cells versus scrambled siRNA control. Experiment Overall Design: Kidney RNA from 3 Dahl salt-sensitive rats was extracted for target preparation and hybridization onto Affymetrix GeneChips. We also isolated kidney RNA from 3 S.LEW(D1MCO4x1x3Bx1) congenic rats for target preparation and hybridization onto Affymetrix GeneChips.
Project description:Kidney samples from three Dahl Salt-sensitive S rats were compared with kidney samples from three S.R(9)x3A congenic rats. Keywords = Blood Pressure Keywords = Quantitative trait locus Keywords = QTL Keywords = hypertension Keywords = rat Keywords = congenic Keywords: parallel sample
Project description:Substitution of chromosome 13 from Brown Norway BN/SsNHsd/Mcw (BN/Mcw) rats into the Dahl salt-sensitive SS/JrHsd/Mcw (SS/Mcw) rats resulted in substantial reduction of blood pressure salt sensitivity in this consomic rat strain designated SSBN13. In the present study, we attempted to identify genes associated with salt-sensitive hypertension by utilizing a custom, known-gene cDNA microarray to compare the mRNA expression profiles in the renal medulla (a tissue playing a pivotal role in long-term blood pressure regulation) of SS/Mcw and SSBN13 rats on either low-salt (0.4% NaCl) or high-salt (4% NaCl, 2 wk) diets. Keywords: Dahl S rat; blood pressure; kidney; consomic rats
Project description:Elevated levels of an endogenous Na/K‐ATPase inhibitor marinobufagenin accompany salt‐sensitive hypertension and are implicated in cardiac fibrosis. Immunoneutralization of marinobufagenin reduces blood pressure in Dahl salt‐sensitive (Dahl‐S) rats. The effect of the anti‐marinobufagenin monoclonal antibody on blood pressure, left ventricular (LV) and renal remodeling, and LV gene expression were investigated in hypertensive Dahl‐S rats.