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 duration of nephropathy, the onset of arterial hypertension (AH), a family history of AH, uric syndrome, intravenous urographic evidence, glomerular filtration rate (GFR) determined from endogenous creatinine, the cellular membranes studied in erythrocytes by ureal hemolysis, and blood levels of thiol and disulfide groups by back amperometric titration, red blood cell activity of glutathione reductase and glucoso-6-phosphate dehydrogenase were evaluated in 108 patients with essential hypertension (EH), mesangial proliferative glomerulonephritis who had elevated and normal blood pressures and 18 healthy subjects. All the patients underwent closed renal puncture biopsy. There were structural alterations in the red blood cell membranes as evidenced by examinations of glucose-6-phosphate dehydrogenase, thiol and disulfide groups in erythrocyte protein and low-weight molecular fractions in healthy subjects with a family history of AH, patients with EH, with mesangial proliferative glomerulonephritis. The abnormal uric syndrome was detected in patients with EH. Patients with AH displayed glomerular hyperfiltration and higher glomerular dimensions. Renal biopsy revealed adrenal interstitial sclerosis in patients with AH.
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PMID:[Arterial hypertension in glomerulonephritis]. 179 79

Oxygen-free radical intermediates/scavengers were measured in 43 patients with essential hypertension who, although under antihypertensive therapy (without angiotensin-converting enzyme inhibitors), still had high blood pressure values. Measurements were taken before and 30, 60 and 120 min after sublingual administration of 25 mg captopril. Both systolic and diastolic blood pressures were reduced significantly. Twenty normotensive healthy volunteers were used as controls. The hypertensive patients had lower glutathione peroxide activity (GSHPx), higher superoxide dismutase (SOD) and serum glutathione reductase activity (GSHRx) compared with the controls. After captopril (30, 60 min) the glutathione and GSHPx increased compared with the pretreatment values. SOD and GSHRx remained high compared with the controls, while whole blood glucose-6-phosphate dehydrogenase remained low. Another group of 19 essential hypertensive patients, free of any antihypertensive medication (for at least 3 weeks), had lower GSHPx, SOD and higher GSHRx than the normal control group. Our results show significant differences in the oxygen free radical scavenger system of hypertensives compared with the normal subjects. It may be that captopril has a concomitant scavenging action together with its antihypertensive effect. Our study raises the question whether cell/organ damage will occur in hypertensive patients exposed to oxidative stress during periods of low antioxidative capacity.
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PMID:Oxygen free radical scavenger system intermediates in essential hypertensive patients before and immediately after sublingual captopril administration. 222 59

Hypertension is accompanied by oxidative stress, which can be modified by the functioning of the endocannabinoid system playing a prominent modulatory role in the brain. The present study tested whether chronic administration of the fatty acid amide hydrolase (FAAH) inhibitor [3-(3-carbamoylphenyl) phenyl]N-cyclohexylcarbamate (URB597) to rats with primary hypertension (SHR) can modify redox balance and consequently brain phospholipid metabolism. Experiments were conducted using SHRs and normotensive control Wistar-Kyoto rats treated by intraperitoneal injection with URB597 for 14 days. The biochemical parameters were assayed in the rats' brains. Inhibition of FAAH activity by URB597 resulted in an increase in anandamide and GPR55 receptor levels, as well as a decrease in CB2 receptor expression. However, there was a simultaneous increase in Nrf2 expression, as well as Cu, Zn-SOD, GSH-Px, glutathione reductase activity, and vitamin E levels in brain tissue of SHR rats. Consequently, URB597 caused a decrease in levels of phospholipid fatty acids and MDA, and an increase in free fatty acids. Given the importance of maintaining redox balance for brain function, the results of this study point to endocannabinoids as a potential therapeutic target for preventing brain metabolic disorders in hypertension.
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PMID:The FAAH Inhibitor URB597 Modulates Lipid Mediators in the Brain of Rats with Spontaneous Hypertension. 3266 25