Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.12.7.2 (hydrogenase)
 3,522 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Results of our previous studies revealed a derangement in the peripheral metabolism of adrenal steroids in patients with essential hypertension. To investigate further this finding, all indIVidual free and conjugated metabolites of cortisol were isolated, identified and quantitated in plasma of 14 normotensive subjects and 13 patients with benign, uncomplicated essential hypertension, following iv administration of a tracer dose of [4-14-C] cortisol. In addition, plasma levels of endogenous cortisol were determined at 8 AM and 4 PM in all the subjects examined. The results obtained revealed the following statistically significant differences between normotensives and hypertensives: 1) Mean plasma concentrations of cortisol metabolites reduced in ring-A with nonreduced 20-ketone, tetrahydrocortisol, tetrahydrocortisone, and their 5alpha-epimers, were 30% lower in the hypertensives; since these steroids constitute the bulk of the major group of cortisol metabolites--the glucuronide conjugates, plasma levels of this group of conjugates measured in toto were also found to be significantly lower in the hypertensives. 2) Concentrations of cortisol metabolites with non-reduced ring-A (delta-4-3-keto configuration preserved) but with reduced 20-ketone and/or hydroxylated at C-6, 20alpha- and 20beta- dihydrocortisol, 6alpha- and 6beta-hydroxycortisol, and 6-hydroxy-20-dihydrocortisol (all 4 isomers), were 73%, 48% and 68% respectively, higher in the hypertensives; since these steroids constitute the bulk of the sulfate-conjugated and nucleoside-complexed metabolites of cortisol, plasma levels of these groups of metabolites, measured in toto, were also found to be higher in the hypertensives. No significant difference was found between normotensives and hypertensives in the AM and PM plasma levels of cortisol. These findings, in conjunction with the results of our studies on urinary corticosteroid metabolites, which yielded identical findings, provide evidence for a decreased activity of hepatic cortisol-delta-4-hydrogenase enzyme system and increased activities (presumably compensatorily) of cortisol-20-reductase and 6-hydroxylase enzyme systems in patients with essential hypertension. The interrelation of these findings with those of other investigators studying steroid metabolites in hypertension, points to the corticosteroid metabolizing enzymes may be an etiological factor in essential hypertension.
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PMID:Corticosteroids in human blood. VIII. Cortisol metabolites in plasma of normotensive subjects and patients with essential hypertension. 113 61

Pregnancy complications have been analyzed in 124 females suffering from essential hypertension (EH) and chronic glomerulonephritis (CGN). Such complications, as late gestosis (8.9%), ablation placentae (1.6%), premature delivery (14.5%), intrauterine growth retardation (14.5%) occurred more frequently than in population. Pre- and perinatal deaths were encountered with the same frequency as in the population. Morphologically, the placentas had in many cases histological evidence of moderate placental insufficiency (PI). In more than 60% of the patients there were uteroplacental and fetoplacental hemodynamic defects. Placental circulatory disorders and PI ran subclinically in most of the cases as they were compensated. In EH and CGN pregnant women, compared to healthy controls, red cells acquired abnormal forms more frequently, serum thromboxane B2 levels got elevated, lactate hydrogenase activity became enhanced. Erythrocytic damage and platelet activation in EH and CGN pregnant women may indirectly confirm the existence of systemic angiopathy. It is suggested that ischemic placenta may produce endothelial toxin, that systemic endothelial damage in EH, CGN, PI may be synergetic which potentiates its clinical appearance in the form of the above pregnancy complications.
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PMID:[The mechanisms of the development of pregnancy complications in hypertension and glomerulonephritis]. 786 44