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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activities of the Na+--K+-ATPase, succinic dehydrogenase (SDH/, lactic dehydrogenase (LDH/ and glucose-6-phosphat dehydrogenase (G-6-PDH/ were studied in the cortex outer and inner medulla of the kidneys of rats with spontaneous hypertension (SHR) and were compared with those of control normotensive Wistar rats. The SHR aged 6--8 weeks had durint the prehypertensive and the early hypertensive stage the same enzymatic activities as control rats. Rats with a steady SH aged 16-22 weeks had low specific activity of the, Na+--K+-ATPase, SDH and LDH in the outer medulla. The latter can be associated with decreased intensity of the energy metabolism and a reduction of the active sodium transport in the ascending limb of the loop of Henle in the SHR rats and cold cause the phenomenon of exaggerated natriuresis characteristic of hypertension.
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PMID:[Na+--K+-adenosine triphosphatase and some oxidoreductases in the kidney of rats with spontaneous hypertension]. 12 6

Some mitochondrial biochemical parameters were determined in Wistar rats with experimentally induced arterial hypertension (AHT) treated with calcium blocking agents of the Verapamil series. The results obtained showed that succinic dehydrogenase (SDH) activity increased, in the group with AHT, by 23.4% as compared with the control group while in the group with AHT treated with Verapamil the activity of this enzyme increased by 46.7%. The NAD+ dehydrogenase activity showed a moderate increase (15.7%) in the group with AHT and an increase by 22.3% after administration of Verapamil. The mitochondrial content in thiolic groups presented an increase of 12.5% in the group with AHT and of 24.4% in the treated group. The kinetics of the mitochondrial swelling-contraction also presented changes in as much as the cycle period, first increased then partially returned to normal values after Verapamil treatment. The strongly stimulating effect of Verapamil on the enzymatic activity in the Krebs cycle was also demonstrated.
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PMID:Effect of calcium blocking agents of the verapamil series on the myocardium mitochondrial activity in experimentally induced arterial hypertension. 129 23

The paper presents a discussion on therapeutic results obtained with plasmapheresis treatment in 16 patients with stage II essential hypertension. Thirty-three comparable patients entered a control group of conventional treatment. The test and control patients with stage II hypertension were examined for time-course changes in T- and B-lymphocytes counts, the activity of the energetic enzymes (alpha-glycerophosphate dehydrogenase, succinic dehydrogenase, lactate dehydrogenase), serum immunoglobulins and circulating immune complex levels. It was established that the standard antihypertensive treatment failed to restore normal parameters of immunity and to favor positive alterations in the activity of the enzymes in the blood lymphocytes, whereas therapeutic plasmapheresis was found to stimulate immunity, especially cellular one. This occurred in line with a rise in the levels of lymphocytic dehydrogenases.
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PMID:[Treatment of patients with hypertonic disease with plasmapheresis]. 281 Dec 12

Activity of some enzymes in the cerebral cortex of rats with experimentally induced renal arterial hypertension (AH) was studied histochemically. Histologic data provide the evidence for the disturbances in water-salt metabolism in AH. Morphometric study revealed an increase in the specific volume of smaller microvessels and moderate decrease in the specific volume of bigger microvessels. Vascular markers show different time course of activity changes in AH: the activity of alkaline phosphatase increases, while that of alpha-glycerophosphate dehydrogenase remains unchanged. The development of AH is accompanied by the increase in succinic dehydrogenase activity and the decrease in the activity of lactate dehydrogenase in neurons. The changes in the neuron-capillary relationship arising in AH can be one of the possible pathogenetic factors in the pathologic process progression.
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PMID:[Characteristics of the morphofunctional status of the tissue in the rat cerebral cortex in experimental renal arterial hypertension]. 366 63

The mechanisms and myocardial alterations associated with NO-deficient hypertension are still far from clear. The aim of the present study was to focus on the enzyme histochemical and subcellular changes in the heart of L-NAME treated rats, as well as to examine the influence of captopril treatment. Wistar rats were administered either L-NAME (40 mg/kg/day) alone or together with captopril (100 mg/kg/day) for a period of 4 weeks. A significant increase of blood pressure confirmed the reliability of the model. The results showed that long-lasting L-NAME administration was accompanied by a decrease of endothelial NO-synthase activity and by a significant local decrease of the following enzyme activities: capillary-related alkaline phosphatase, 5'-nucleotidase and ATPase (but not dipeptidyl peptidase IV) and cardiomyocyte-related glycogen phosphorylase, succinic dehydrogenase, beta-hydroxybutyrate dehydrogenase and ATPases. No activity of these enzymes was found in the scar, whereas a marked increase of alkaline phosphatase and dipeptidyl peptidase IV activities was found in the foci of fibrotization. Histochemical changes correlated with subcellular changes, which were characterized by 1) apparent fibroblast activation associated with interstitial/perivascular fibrosis, 2) heterogeneous population of the normal, hypertrophic and injured cardiomyocytes, 3) enhancement of the atrial granules and their translocation into the sarcolemma, and 4) impairment of capillaries as well as by induction of angiogenesis. Similar alterations were also found in the heart of captopril co-treated rats, despite of the significant suppression of blood pressure. The results indicate that NO-deficient hypertension is accompanied by metabolic disturbances and ultrastructural alterations of the heart and these changes are probably not induced by the renin-angiotension system only.
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PMID:Chronic disturbances in NO production results in histochemical and subcellular alterations of the rat heart. 1080 8

These investigations are part of an attempt to study and interpret the intermediary metabolism of the kidneys in experimental renal hypertension. Hypertension was produced in dogs by the clamping procedure of Goldblatt and associates or by the silk perinephritis method of Page. Enzymatic studies were made by means of Warburg's manometric method. Cytochrome c was in addition determined spectrophotometrically. Tissue slices, homogenized tissue, and tissue extracts were used. A study of the cytochrome c concentration and the activities of the cytochrome oxidase and succinic dehydrogenase systems of kidneys from normal dogs and dogs with experimental renal hypertension was made. It was found that the cytochrome c concentration and the activities of the cytochrome oxidase and succinic dehydrogenase systems were markedly lower in the kidney slices and in the tissue suspensions from hypertensive dogs. Tissue suspensions and extracts of kidneys from hypertensive dogs showed an inhibitory effect on the activity of the cytochrome oxidase and succinic dehydrogenase, and the amine oxidase systems. Renin preparations also showed a marked inhibitory effect on the activities of cytochrome oxidase, succinic dehydrogenase, l-amino acid oxidase, and amine oxidase systems. A significant increase was found in the kidney of dogs whose other kidney had been removed or subjected to Goldblatt's or Page's technique in the activities of the cytochrome-cytochrome oxidase system, the succinic dehydrogenase system, and in the concentration of nucleotide-bound phosphorus, of flavin-adenine dinucleotide, and of the nicotinamide-adenine dinucleotides (coenzymes I and II). From the results of these studies it can be concluded that an increase in the concentration and activity of the respiratory enzymes precedes hypertrophy of the kidney. This can be explained by the assumption that an increase in the activity of the respiratory biocatalysts acts as a stimulus for cell growth and multiplication.
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PMID:THE METABOLISM OF THE KIDNEY IN EXPERIMENTAL RENAL HYPERTENSION : II. THE CONCENTRATION OF CYTOCHROME C AND THE ACTIVITIES OF THE CYTOCHROME OXIDASE AND OF THE SUCCINIC DEHYDROGENASE SYSTEMS IN THE KIDNEY OF DOGS WITH EXPERIMENTAL RENAL HYPERTENSION. THE INHIBITORY EFFECT OF RENIN AND OF KIDNEY TISSUE PREPARATIONS FROM HYPERTENSIVE DOGS ON THE RESPIRATORY ENZYMES. 1987 97