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

The energy metabolism of cardiac hypertrophy in spontaneously hypertensive rats (SHR) was studied chronologically by histochemical and in part chemical methods. The activities of various enzymes, such as glucose-6-phosphate dehydrogenase (G6PDH), lactate dehydrogenase (LDH), isocitrate dehydrogenase, succinate dehydrogenase, beta-hydroxybutylate dehydrogenase (beta-HBDH) and monoamine oxidase (MAO) in the cardiac muscle were determined histochemically. beta-HBDH activity was greatly increased in the stage of developing hypertension in SHR. LDH activity increased simultaneously with the rise of beta-HBDH activity. Moreover, MAO activity increased markedly in later stages when the blood pressure was already elevated in SHR. To confirm the histochemical findings of beta-HBDH activity, the mitochondrial fraction of cardiac muscle was subjected to chemical assay. The chemical findings of myocardial beta-HBDH in SHR corresponded well with the histochemical findings. The myocardial beta-HBDH activity in SHR increased markedly at the age of 5 to 9 weeks, while no or minimal activity was found in controls of the same age. No significant difference of beta-HBDH activity was observed between SHR and controls in the mitochondrial fraction from the diaphragm and liver. The increase of beta-HBDH activity in the cardiac muscle of SHR prior to the development of cardiac hypertrophy suggests that the metabolism of ketone bodies may play an important role in providing the energy necessary for the development of cardiac hypertrophy in SHR.
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PMID:Cardiac hypertrophy in spontaneously hypertensive rats. 12 86

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

The activity of succinate dehydrogenase, alpha-glycerophosphate dehydrogenase and acid phosphatase in the lymphocytes of peripheral blood was studied in 28 patients with hypertensive disease and vasorenal hypertension (the diagnosis was made on the basis of the findings of angiographic examination) by the method of quantitative cytochemical analysis suggested by R.P. Nartsissov. It was revealed that alpha-glycerophosphate dehydrogenase activity was significantly lower in vasorenal hypertension than in hypertensive disease. The calculation of the difference between the value of succinate dehydrogenase activity and that of alpha-glycerophosphate dehydrogenase activity in these groups was also significant. It is concluded that a complex of cytochemical analysis may be used in differential diagnosis of vasorenal hypertension and hypertensive disease.
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PMID:[Determination of dehydrogenase and acid phosphatase activity in the lymphocytes in hypertension and vasorenal hypertension]. 72 32

The specific activities (S.A.) of the succinate dehydrogenase-coenzyme Q10 (CoQ10) reductase of a control group of 65 Japanese adults and 59 patients having essential hypertension were determined. The mean S.A. of the hypertensive group was significantly lower (p less than 0.001) and the mean % deficiency of enzyme activity was significantly higher (p less than 0.001) than the values for the control group. These data on Japanese in Osaka agree with data on Americans in Dallas. Some patients showed no CoQ10-deficiency, and others showed definite deficiencies. Emphasizing the CoQ10-enzyme for patient selection, CoQ10 was administered to hypertensive patients. Four individuals showed significant but partial reductions of blood pressure. Monitoring the CoQ10-enzyme before, during, and after administration of CoQ10 indicated responses. The maintenance of high blood pressure could be primarily due to contraction of the arterial wall. Contraction or relaxation of an arterial wall is dependent upon bioenergetics, which also provide the energy for biosynthesis of angiotensin II, renin, aldosterone, and the energy for sodium and potassium transport. A clinical benefit from administration of CoQ10 to patients with essential hypertension could be based upon correcting a deficiency in bioenergetics, and point to possible combination treatments with a form of CoQ and anti-hypertensive drugs.
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PMID:Bioenergetics in clinical medicine. Studies on coenzyme Q10 and essential hypertension. 115 73

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

A quantitative histochemical study of succinate dehydrogenase (SDH) and NADH-dehydrogenase (NADH-D) activity in medulla oblongata structures was accomplished in rats with arterial renovascular hypertension of the "2 kidneys-2 clips" type lasting 5 months. The systolic arterial blood pressure measured by the tail-cuff method was 179 +/- 4 mm Hg in hypertensive rats versus 108 +/- 3 mm Hg in control. There was a significant elevation of SDH activity in the ventral reticular and commissural nuclei, while in the neurons of the vagus dorsal and ambiguous nuclei it was lowered. NADH-D activity was significantly increased in the neuropil of the hypoglossal nerve nucleus and reduced in its neurons. The general trend was also revealed toward reduction of the maximal and elevation of the minimal activities in other nuclei. These metabolic alterations reflect changes in the functional activity of vasomotor and other structures of the medulla oblongata in renovascular hypertension.
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PMID:[Functional activity of the structures of the medulla oblongata in rats with arterial hypertension of renal origin (histoenzymological research)]. 401 28

The subcellular distribution and nature of rat renal renin has been investigated by means of analytical subcellular fractionation and gel filtration on Sephadex G-100. During differential centrifugation, renin activity was recovered mainly in soluble and heavy mitochondrial fractions. On sucrose gradient centrifugation in either a conventional or in a B XIV zonal rotor, renin activity equilibrated at 1.54 M sucrose and was partially resolved from marker enzymes for mitochondria (succinate dehydrogenase), lysosomes (acid phosphatase), plasma membranes (alkaline phosphatase), and peroxisomes (catalase). On gel filtration of the soluble or extracts of the renin-granular fractions on Sephadex G-100, renin activity eluted as a single peak with an apparent molecular weight (MW) of 42,000; no change in activity was found when these fractions were acidified to pH 3.0. When kidney homogenates were prepared in the presence of the proteolytic inhibitor N-ethylmaleimide (NEM, 10 mM), whereas the renin from the granular fractions displayed a MW of 44,000, that from the soluble fraction was apparently higher (69,000). Addition of NEM (10 mM) to the soluble fraction previously shown to contain only the low MW form of renin also resulted in an apparently high MW form of renin. These results indicate that rat renal renin is associated with a mechanically fragile, distinct type of subcellular organelle. Renin within this structure is of the low MW form and is not acid activatable. The soluble fraction, however, contains a factor(s) that, in the presence of NEM, combines with the low MW renin to form a complex of apparently high MW.
Hypertension
PMID:Subcellular distribution and storage form of rat renal renin. 699 67

Cytochemical analysis was used to compare the activities of hyaloplasmatic and mitochondrial glycerophosphate dehydrogenase, and succinate dehydrogenase in lymphocytes of peripheral blood taken from 14 aviators with the diagnose of hypertonic neurocirculatory dystonia, and 18 healthy aviators. Significantly higher activity of these enzymes in patients is assumed to signify intensification of metabolism and cellular respiration bearing the forced adaptive character. On this evidence, an attempt is made to interpret earlier discovered changes in the immunobiochemical status of these patients and plausible mechanisms of progressive arterial hypertension are hypothesized. Emphasis is laid on the necessity to direct secondary preventive measures at the early phases of hypertension not only on reduction of the vascular tone and correction of the immunobiochemical status but on building-up of cell's functional reserves.
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PMID:[Some mechanisms of pathogenesis of hypertonic type neurocirculatory dystonia in flying personnel]. 896 66


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