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)

Pharmacokinetic parameters-including tissue distribution, biliary excretion, and urinary excretion of M1-M4-were compared after an intravenous administration of DA-125 (a new anthracycline derivative; 20 mg/kg body weight) to male spontaneously hypersensitive rats (SHRs) at 16 weeks (an animal model for human primary hypertension) and at 6 weeks (corresponding to the early phase of the development of hypertension, at which time blood pressure remains within the normotensive range) of age and their age-matched control Kyoto-Wistar rats, and male deoxycorticosterone acetate-salt-induced Sprague-Dawley rats (DOCA-salt rats, an animal model for human secondary hypertension) at 16 weeks of age and their age-matched control Sprague-Dawley rats. Mean plasma concentrations of both M2 and M4, and the resultant area under the plasma concentration-time curve from time 0 to last measured time [AUCT; M2 (68.9 vs. 29.3 micrograms-min/ml) and M4 (53.4 vs. 33.4 micrograms-min/ml)], increased significantly in SHRs at 16 weeks of age, compared with their control rats. Similar results were also obtained from DOCA-salt rats at 16 weeks of age, compared with their control rats. However, values were not significantly different between SHRs at 6 weeks of age and their control rats. Previous data indicated that the significant increase in plasma concentrations and the resultant AUCT values of both M2 and M4 in SHRs at 16 weeks of age were due to the hypertension state itself, and not to any hereditary characteristics of the SHRs. The significantly increased plasma concentrations and the resultant AUCT values of M2 in both SHRs and DOCA-salt rats at 16 weeks of age were due to the significantly decreased biliary excretion of M2 and possibly to the increased amount of aldo-keto reductase in the liver. However, the increase in the two aforementioned pharmacokinetic parameters in the case of M4 were possibly due solely to the increased amount of aldo-keto reductase in the liver.
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PMID:Pharmacokinetics of DA-125, a new anthracycline, after intravenous administration to spontaneously hypertensive rats and DOCA-salt-induced hypertensive rats. 901 Jun 32

Aldose Reductase (AR), encoded by AKR1B1, is a member of NADPH-dependent aldo-keto reductase superfamily. The C-106T polymorphism of AKR1B1 is closely related to the diabetic complications. Our previous studies have indicated that the expression of AR was increased in spontaneously hypertensive rats, suggesting the effect of AR in hypertension. Here we investigated whether AKR1B1 C-106T polymorphism was associated with essential hypertension (EH). AKR1B1 C-106T polymorphism was genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and the direct sequencing methods. 383 healthy subjects and 383 essential hypertensive patients were recruited in this study. The polymorphism of AKR1B1 C-106T in EH and normal tensive (NT) groups was in agreement with Hardy-Weinberg equilibrium. -106T allele of AKR1B1 C-106T variants was more frequent in EH patients compared with normal tensive subjects, indicating that -106T allele was a risk factor of EH (OR=1.841, 95%CI=1.366-2.481). In male patients, C-106T polymorphism was associated significantly with decreased serum high density lipoprotein cholesterol and higher systolic blood pressure levels. Our results suggest that -106T allele of AKR1B1 C-106T polymorphism may be associated with increased risk for EH in Chinese Han population.
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PMID:Aldose reductase C-106T polymorphism is associated with the risk of essential hypertension. 2734 77