Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression Profiling of Genes Concerning to Protective Effect in Heart by Benidipine Hydrochloride.

ABSTRACT: Benidipine hydrochloride is a long-acting calcium channel blocker and is used for the treatment of hypertension and angina pectoris. The cardioprotective effects of benidipine have been shown in several animal and clinical studies. We examined the effect of the dihydropyridine calcium channel blocker (CCB) benidipine on the gene expression profile in heart by DNA microarray. Dahl salt-sensitive (DS) rats were fed with normal diet (0.19% NaCl) or a high-salt diet (8% NaCl) from 7 weeks of age. Benidipine (4mg/kg) or vehicle (0.5% w/v methylcellulose 400cP) was administered orally after the start of the feeding. DS rats fed the high-salt diet showed an increase in systolic blood pressure (SBP), which was accompanied by the gain of heart weight. SBP was significantly lower in the benidipine group than in the vehicle group. The weight of heart was significantly decreased in the benidipine group. Keywords: Diseased state and drug effect analysis

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE8201 | GEO | 2009/06/16

SECONDARY ACCESSION(S): PRJNA101111

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of rat Dahl salt sensitive strain heart treated with dihydropyridine calcium channel blocker (CCB) benidipine.

Project description:Benidipine hydrochloride is a long-acting calcium channel blocker and is used for the treatment of hypertension and angina pectoris. The cardioprotective effects of benidipine have been shown in several animal and clinical studies. We examined the effect of the dihydropyridine calcium channel blocker (CCB) benidipine on the gene expression profile in heart by DNA microarray. Dahl salt-sensitive (DS) rats were fed with normal diet (0.19% NaCl) or a high-salt diet (8% NaCl) from 7 weeks of age. Benidipine (4mg/kg) or vehicle (0.5% w/v methylcellulose 400cP) was administered orally after the start of the feeding. DS rats fed the high-salt diet showed an increase in systolic blood pressure (SBP), which was accompanied by the gain of heart weight. SBP was significantly lower in the benidipine group than in the vehicle group. The weight of heart was significantly decreased in the benidipine group. Experiment Overall Design: Three samples were analyzed, the hearts of rat with normal diet (normal), high-salt diet plus vehicle (control), high-salt diet plus Benidipine (Benidipine). We use 2 arrays: control vs. normal and Benidipine vs. control. Replicates and dye swaps were not performed.

2009-06-23 | E-GEOD-8201 | biostudies-arrayexpress

Mechanisms of Sinoatrial Node Dysfunction in Heart Failure with Preserved Ejection Fraction

Project description:RNA sequencing from sinoatrial node tissue was performed to identify transcriptomic changes in Dahl salt-sensitive rats fed with normal salt diet (0.4% NaCl, control group) or high-salt diet (8% NaCl, HFpEF group) for 11 weeks. Transcriptomic profiling revealed numerous changes in multiple disease-associated genes in HFpEF, which is functionally related to the observed physiological impairments and structural remodeling.

2022-05-18 | GSE184120 | GEO

Transcription profiling of rat kidney samples from Dahl salt-sensitive and Lewis strains

Project description:Male Dahl salt sensitive and Lewis rats (n=3 each) were fed an 8% NaCl diet starting at 5 weeks of age for 8 weeks. Total RNA was isolated with TRIzol reagent from DS and LEW kidneys and was subjected to microarray analysis. Experiment Overall Design: Male Dahl salt sensitive and Lewis rats (n=3 each) were fed an 8% NaCl diet starting at 5 weeks of age for 8 weeks. Total RNA was isolated with TRIzol reagent from DS and LEW kidneys and was subjected to microarray analysis. The resulting data were analyzed with GeneChip Operating Software ver1.4. Three independent experiments comparing expressions between salt-loaded Dahl salt sensitive and salt-loaded Lewis rats were performed.

2007-11-29 | E-GEOD-4800 | biostudies-arrayexpress

TMC4 is a novel chloride channel involved in high-concentration salt taste sensation

Project description:Taste substances are received by taste receptors expressed in taste cells. “Salty taste” sensation is evoked when sodium and chloride ions are present together in the oral cavity. The presence of an epithelial cation channel that receives Na+ has previously been reported. However, no molecular entity involving Cl- receptors has been elucidated. We report the strong expression of transmembrane channel-like 4 (TMC4) in the circumvallate and foliate papillae projected to the glossopharyngeal nerve, mediating a high-concentration of NaCl. Electrophysiological analysis using HEK293T cells revealed that TMC4 was a voltage-dependent Cl- channel and the consequent currents were completely inhibited by NPPB, an anion channel blocker. This channel could be activated without an increase in intracellular calcium ion. TMC4 allowed permeation of organic anions including gluconate, but their current amplitudes at positive potentials were less than that of Cl-. Tmc4-deficient mice showed significantly weaker glossopharyngeal nerve response to high-concentration of NaCl than the wild-type littermates. These results indicated that TMC4 is a novel chloride channel that responds to high-concentration of NaCl.

2021-09-14 | GSE175806 | GEO

Gene expression in kidney from Lewis and Dahl(S) rat

2007-05-09 | GSE4800 | GEO

Transcriptomic response in the heart and kidney to different types of antihypertensive drug administration

Project description:To unravel antihypertensive drug-induced gene expression changes that are potentially related to the amelioration of end-organ damages, we performed in vivo phenotypic evaluation and transcriptomic analysis on the heart and the kidney, with administration of antihypertensive drugs to two inbred strains of (i.e., hypertensive and normotensive) rats. We chose to use six antihypertensive classes: enalapril (angiotensin converting enzyme inhibitor), candesartan (angiotensin receptor blocker), hydrochlorothiazide (diuretics), amlodipine (calcium-channel blocker), carvedilol (vasodilating -blocker) and hydralazine. In the tested rat strains, four of six drugs, including two renin-angiotensin system (RAS) inhibitors, were effective for BP lowering, whereas the remaining two drugs were not. Besides BP lowering, there appeared to be some inter-drug heterogeneity in phenotypic changes, such as suppressed body weight (Bw) gain and Bw-adjusted heart weight reduction. For the transcriptomic response, a considerable number of genes showed prominent mRNA expression changes either in a BP-dependent or BP-independent manner with substantial diversity between the target organs. Noticeable changes of mRNA expression were induced particularly by RAS blockade, e.g., for genes in the natriuretic peptide system (Nppb and Corin) in the heart and for those in the RAS/ kallikrein-kinin system (Ren and rat Klk1 paralogs) and those related to calcium ion binding (Calb1 and Slc8a1) in the kidney. The heart data comprises of this submission and part of E-MTAB-9244.

2022-04-15 | E-MTAB-10667 | biostudies-arrayexpress

Physiologic cardiac hypertrophy

Project description:Dahl salt-sensitive (DS) rats were obtained from Harlan Sprague Dawley Laboratory at 5 weeks of age. At 6 weeks of age, physiologic cardiac hypertrophy was generated by a vigorous daily exercise regimen for 6 weeks (e group). The exercise protocol is based on those described previously with modifications (Wisloff U et al., 2001; Jin H et al., 1994). Rats were exercised daily for 6 weeks on a rodent treadmill (Exer-6M; Columbus Instruments). The exercise program consisted of three weeks of progressively strenuous exercise regimens; followed by three weeks of maintenance period, during which the rats were exercised at 16 m/min at a 5o incline for 90 minutes/day. All rats completed the exercise protocol. Pathological cardiac hypertrophy was generated by feeding a 6% NaCl diet to DS rats at 6 weeks of age (h group) (Inoko M et al., 1994). Control rats (c group) were age matched and sedentary DS rats fed normal rat chow. Read more at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/rat_home.html Keywords: other

2003-10-24 | GSE776 | GEO

Transcriptomic response in the heart and kidney to different types of antihypertensive drug administration

Project description:To unravel antihypertensive drug-induced gene expression changes that are potentially related to the amelioration of end-organ damages, we performed in vivo phenotypic evaluation and transcriptomic analysis on the heart and the kidney, with administration of antihypertensive drugs to two inbred strains of (i.e., hypertensive and normotensive) rats. We chose to use six antihypertensive classes: enalapril (angiotensin converting enzyme inhibitor), candesartan (angiotensin receptor blocker), hydrochlorothiazide (diuretics), amlodipine (calcium-channel blocker), carvedilol (vasodilating beta-blocker) and hydralazine. In the tested rat strains, four of six drugs, including two renin-angiotensin system (RAS) inhibitors, were effective for BP lowering, whereas the remaining two drugs were not. Besides BP lowering, there appeared to be some inter-drug heterogeneity in phenotypic changes, such as suppressed body weight (Bw) gain and Bw-adjusted heart weight reduction. For the transcriptomic response, a considerable number of genes showed prominent mRNA expression changes either in a BP-dependent or BP-independent manner with substantial diversity between the target organs. Noticeable changes of mRNA expression were induced particularly by RAS blockade, e.g., for genes in the natriuretic peptide system (Nppb and Corin) in the heart and for those in the RAS/ kallikrein-kinin system (Ren and rat Klk1 paralogs) and those related to calcium ion binding (Calb1 and Slc8a1) in the kidney. This submission includes the kidney data.

2022-04-15 | E-MTAB-10672 | biostudies-arrayexpress

Dietary salt and renal function

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

2004-02-14 | GSE599 | GEO

Effect of calcium depletion on cold induced gene expression in barley

Project description:Agilent 44k barley microarray was used to screen calcium dependent cold induced genes. Calcium chelator (EGTA) or calcium channel blocker (lanthanum) or phospholipase C activator (mastoparan) pretreatments were performed to block/enhance calcium response in barley seedlings. Calcium depleted and control plants were cold treated and the difference in the gene expression was investigated.

2014-12-31 | GSE47432 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data