Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of the present study was to assess the relationship between microalbuminuria (Malb) and left ventricular hypertrophy (LVH), when levels of ambulatory BP was token in to account as a confounder factor. Patients with essential hypertension, aged 25 to 50 years old, never treated with antihypertensive drugs, were included in the study. The inclusion criteria were: (a) absence of diabetes, renal disease or urinary tract infection; (b) urinary albumin excretion (UAE) estimated in urine of 24 hours in two separate days; (c) echocardiography suitable for measurement of left ventricular mass (LVM); and (d) good quality ambulatory blood pressure monitoring during 24 hours. UAE was measured using a immunonephelometric assay (Behring Institute) and Malb was considered when UAE 30 to 300 mg/24 hours during the two days. LVM was calculated by the Devereaux formula and referred to height (LVMI g/m). AMBP was performed using an oscilometric device (Spacelabs 90202 or 90207) during a regular working day. Readings were programmed every 20 minutes between 6 a.m. to midnight and thereafter every 30 minutes. The average BP during a 24 hour period was calculated. One hundred and fifty one patients (96 male, mean age 37 +/- 8 years, body mass index 27.7 +/- 3.7 g/m2) were included. The average values of office BP was 148 +/- 15/96 +/- 8 mm Hg, and the average BP during 24 hours was 137 +/- 13/88 +/- 12 mm Hg. UAE was 30.1 +/- 52.3 mg/24 hr and the LVMI 140.6 +/- 44.1 g/m. The percentage of Malb patients was 28% and those with LVH 34%. A significant relationship between UAE and office and ambulatory SBP and DBP was observed. LVMI was also significantly related to ambulatory SBP and DBP, a relationship that was not found for office BP. In a multiple regression model, significant relationship between UAE and LVMI emerged, independent of diastolic ambulatory BP, age and sex (P < 0.04). In conclusion; we observed a significant relationship between UAE and LVMI, in part, independent of blood pressure. The fact that Malb is associated with the presence of LVH, supports the idea that Malb is a risk marker in essential hypertensive patients.
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PMID:Microalbuminuria, left ventricular mass and ambulatory blood pressure in essential hypertension. 874 18

The kidney has long been invoked in the etiology of essential hypertension. This could involve alterations in expression of specific genes and microRNAs (miRNAs). The aim of the present study was to identify, at the transcriptome-wide level, mRNAs and miRNAs that were differentially expressed between kidneys of 15 untreated hypertensive and 7 normotensive white male subjects of white European ancestry. By microarray technology we found 14 genes and 11 miRNAs that were differentially expressed in the medulla. We then selected and confirmed by real-time quantitative PCR expression differences for NR4A1, NR4A2, NR4A3, PER1, and SIK1 mRNAs and for the miRNAs hsa-miR-638 and hsa-let-7c. Luciferase reporter gene experiments in human kidney (HEK293) cells confirmed the predicted binding of hsa-let-7c to the 3' untranslated region of NR4A2 mRNA. In the renal cortex we found differential expression of 46 genes and 13 miRNAs. We then confirmed expression differences for AIFM1, AMBP, APOE, CD36, EFNB1, NDUFAF1, PRDX5, REN, RENBP, SLC13A1, STX4, and TNNT2 mRNAs and for miRNAs hsa-miR-21, hsa-miR-126, hsa-miR-181a, hsa-miR-196a, hsa-miR-451, hsa-miR-638, and hsa-miR-663. Functional experiments in HEK293 cells demonstrated that hsa-miR-663 can bind to the REN and APOE 3' untranslated regions and can regulate REN and APOE mRNA levels, whereas hsa-miR-181a regulated REN and AIFM1 mRNA. Our data demonstrated for the first time that miRNAs can regulate renin expression. The observed downregulation of 2 miRNAs in hypertension could explain the elevation in intrarenal renin mRNA. Renin, CD36, and other mRNAs, as well as miRNAs and associated pathways identified in the present study, provide novel insights into hypertension etiology.
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PMID:Gene expression profiling reveals renin mRNA overexpression in human hypertensive kidneys and a role for microRNAs. 2204 11