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

Plasma cholesterol was lower in spontaneously hypertensive rats (SHR), while plasma triglyceride and free fatty acid were increased in comparison with control normotensive Wistar-Kyoto (WK) rats. Correspondingly, [1-14C]-acetate incorporation into liver cholesterol was clearly decreased in SHR as compared with WK. As for lipogenic enzyme activities, glucose-6-phosphate dehydrogenase, malic enzyme and acetyl-CoA carboxylase in SHR were respectively decreased, increased and not significantly different, in comparison with WK rats. Liver cholesterol was rather low and cardiac triglyceride was slightly increased in SHR. Aortic cholesterol and triglyceride levels were not significantly different between SHR AND WK rats. Thus, SHR have an abnormality in lipid metabolism, especially in cholesterol synthesis, but the pathological implication of this in hypertension and related vascular lesions is not yet clear.
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PMID:Lipid metabolism in spontaneously hypertensive rats (SHR). 2 30

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

Approximately 13 percent of American Negro males carry a mutant [A-variant] glucose-6-phosphate dehydrogenase enzyme in their red blood cells that predisposes them to hemolytic episodes following exposure to oxidant drugs such as primaquine. Most hemolytic episodes to standard prophylactic treatment are mild and self-limited, but as many as 2 percent of Negro males develop severe hemolysis when similarly treated. The exaggerated response may be due in part to the combination of G-6-PD deficiency and hypertension since hypertension can cause red cell fragmentation, and the stressed cells of G-6-PD deficient person would be more sensitive to such fragmentation.
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PMID:The possible role of hypertension in aggravating hemolytic episodes in G-6PD deficient persons. 37 56

Plasma from normal humans and rats on a high sodium intake, and from patients and rats suffering from hereditary hypertension has an increased cytochemically detectable glucose-6-phosphate dehydrogenase (G6PD)-stimulating/Na-K-ATPase inhibiting activity. The hypothalamic content of this activity is also increased by a high sodium intake and in the spontaneously hypertensive rat (SHR). Using cytochemical techniques, the ability of plasma and the hypothalamus of reduced renal mass hypertensive rats to stimulate G6PD activity and to inhibit Na-K-ATPase was measured. The mean G6PD-stimulating capacity of the plasma from the hypertensive and normotensive groups of rats was 351 +/- 67 and 11.42 +/- 1.98 G6PD-stimulating units/mL respectively (P less than .001). The time courses of the ability of plasma from a hypertensive and a normotensive rat to inhibit fresh tissue Na-K-ATPase after 2, 4, 6, and 8 min of exposure demonstrated that the hypertensive rat plasma had a greater capacity to inhibit Na-K-ATPase. The mean G6PD-stimulating capacity of the hypothalamus from the hypertensive and normotensive groups of rats was 252,263 +/- 147,958 X 10(3) and 6.38 +/- 2.35 X 10(3) G6PD-stimulating units per hypothalamus, respectively (P less than .01). It is proposed that the raised concentration of cytochemically detectable G6PD-stimulating/Na-K-ATPase-inhibiting substance in both genetic and nongenetic forms of hypertension may be a manifestation of a communal hypertensinogenic mechanism. Thus, the raised plasma concentration would have a direct peripheral vascular constricting effect and the high hypothalamic concentration would be responsible for a central nervous hypertensinogenic effect.
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PMID:Cytochemically detectable glucose-6-phosphate dehydrogenase-stimulating/Na-K-ATPase-inhibiting activity of plasma and hypothalamus in reduced renal mass hypertension. 164 96

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

The ability of plasma from 3- and 9-week-old Milan hypertensive rats and their normotensive controls to inhibit Na+,K+-adenosine triphosphatase (ATPase) was studied using cytochemical bioassay techniques in fresh tissue. With a validated cytochemical bioassay that measures the capacity of biological samples to stimulate glucose-6-phosphate dehydrogenase activity in guinea pig proximal tubules as an indication of their capacity to inhibit Na+,K+-ATPase, the mean glucose-6-phosphate dehydrogenase-stimulating ability of the plasma of the 9-week-old Milan hypertensive rats and their normotensive controls was 586.0 +/- 88 and 23.4 +/- 8.3 U/ml (n = 7; p less than 0.001), while that of the 3-week-old Milan hypertensive rats (before the main rise in arterial pressure) and their normotensive controls was 99.9 +/- 27.4 and 7.8 +/- 1.8 U/ml (n = 7; p less than 0.001). With the use of a semiquantitative cytochemical assay that measures Na+,K+-ATPase activity directly, plasma from the adult hypertensive rats had a much greater capacity to inhibit Na+,K+-ATPase than the plasma of the control rats. The significantly raised levels found in the young hypertensive rats before the main rise in arterial pressure are consistent with the hypothesis that the rise in the ability of plasma to inhibit Na+,K+-ATPase is due to an inherited renal difficulty in excreting sodium.
Hypertension 1987 May
PMID:Cytochemically assayable Na+,K+-ATPase inhibition by Milan hypertensive rat plasma. 303 90

Biochemical, cytochemical and immunological methods were used to compare the metabolic and neuroendocrine properties of the subfornical organ (SFO) with the hypothalamo-neurohypophysial system (HNS) in the rat. The SFO resembles the HNS in that both have (a) increased label incorporation into RNA during dehydration; (b) an intense reaction for glucose-6-phosphate dehydrogenase; (c) NADPH-diaphorase and the Type I pathway for hydrogen utilization from NADPH, presumably as part of the mixed-function oxidase system for the metabolism of endogenous substrates and xenobiotics; (d) immunoreactive vasopressin and oxytocin. Gel filtration of extracts of the SFO area using Sephadex G-25 chromatography resulted in immunoreactive peaks for both AVP and OT which were similar to synthetic hormones. One other fraction in the SFO extract, containing a substance(s) of higher molecular weight than AVP, was detected using the antiserum for AVP. The concentration of immunoreactive AVP in the SFO area was increased after colchicine, decreased by hypophysectomy, and unaltered by: (a) infusion (4.6 pg/min for 3 hr) or injection (1 or 6 ng) of AVP into the lateral cerebroventricle; (b) dehydration; (c) renin administered intracerebroventricularly; (d) pinealectomy; or (e) hypertension in the spontaneously hypertensive rat. In conclusion, cells in the SFO have specialized metabolic and neuroendocrine properties similar to the HNS. It can be inferred from these biochemical specializations that the SFO has metabolic and secretory activities.
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PMID:The subfornical organ: biochemical and neuroendocrine comparisons with the hypothalamo-neurohypophysial system. 402 8

To assess the oxidative stress across the cell membrane in patients suffering from pregnancy induced hypertension, erythrocyte malonyldialdehyde, vitamin E, reduced glutathione, glucose-6-phosphate dehydrogenase activity and plasma urate levels were estimated in 25 non pregnant women, 40 normotensive pregnant women and 40 women with pregnancy induced hypertension (PIH). As compared to non pregnant women, there was a significant increase in the levels of erythrocyte malonyldialdehyde and plasma urate in normotensive pregnant women, which were further increased in women with PIH. Erythrocyte glutathione levels were raised in normotensive pregnant women as compared to non pregnant women. Its levels were decreased in patients of PIH as compared to normotensive pregnant women. Cellular bio-availability of vitamin E was depressed in both normotensive pregnancy as well as patients with pregnancy induced hypertension as compared to non pregnant women.
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PMID:Levels of erythrocyte malonyldialdehyde, vitamin E, reduced glutathione, G6PD activity & plasma urate in patients of pregnancy induced hypertension. 792 48

Toxicosis syndrome of fasting pregnant ewes has a close similarity to human preeclampsia (hypertension, albuminuria). The common etiological factor might be oxidative hemolysis and heme-induced endothelial damage. Ewes (5 starving, 5 control) at 130-135 gestational days with a 96-h fasting period followed by refeeding were used. Blood pressure, platelet count, electrolytes, kidney and liver function parameters, as well as plasma glucose, hemoglobin/heme, free thiol groups and Trolox equivalent antioxidant capacity, and plasma iron and ferritin levels were measured. Statistical significance was assessed using Student's t test (P < 0.05). Besides hypertension and renal disturbances, hemolysis, elevated liver enzymes and low platelet count, characteristic of human HELLP syndrome, were also present. In the first 24 h of glucose deprivation there was a significant rise in both the plasma hemoglobin/heme and indirect bilirubin concentrations. The antioxidant free thiol levels decreased significantly the next day, without any change in the total antioxidant capacity of the plasma. While the loss of calcium and magnesium levels related to the similarity to preeclampsia, reduced plasma iron concentrations referred to species differences in iron homeostasis. An oxidative stress causing hemolysis in a glucose-6-phosphate dehydrogenase-deficient animal model was proven by the loss of free thiols after glucose deprivation. The activation of the oxidative stress protein heme oxygenase was a signal of endothelial cell injury, the primary cause of pregnancy-induced hypertension.
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PMID:The pathogenetic role of heme in pregnancy-induced hypertension-like disease in ewes. 936 99


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