Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Robust sib-pair linkage analysis can be used as a screening tool in the search for the potential involvement of single-loci, multiple-loci, and pleiotropic effects of single loci underlying phenotypic variation. Four large families were each ascertained through one adult white male with essential hypertension. The robust sib-pair method was used to screen these families for evidence of linkage between 39 quantitative traits related to hypertension and 25 genetic marker loci. All traits were analyzed on the untransformed, square-root and log-transformed scales. Among other findings, there is a suggestion of linkage between the 6-phosphogluconate dehydrogenase locus on chromosome 1p36 and mean fifth-phase diastolic blood pressure. There may also be linkage between the following markers and traits: the adenylate kinase-1 marker and/or the Lewis blood group marker and the traits height, weight, and biacromial breadth; the glyoxylase I marker and the traits upper-arm circumference and suprailiac skinfold thickness; the ABO blood group and adenylate kinase-1 markers on chromosome 9q34 and the third component of complement marker on chromosome 19p13 and dopamine-beta-hydroxylase; and the P1 blood group and the traits weight and 1-h postload serum glucose level.
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PMID:Use of the robust sib-pair method to screen for single-locus, multiple-locus, and pleiotropic effects: application to traits related to hypertension. 201 38

A follow-up study of muscle strength, muscle morphology, and enzymatic activity in 23 men, 73-83 years of age, was performed 7 years after the first investigation. With the exception of two men treated for congestive heart failure and four treated for hypertension, all were apparently clinically healthy and none had functional locomotor disturbances. Body weight was reduced by 2% and body cell mass by 6%, whereas the quadriceps muscle strength decreased 10%-22% over the 7-year period. Fiber composition in the vastus lateralis did not change significantly, and there was no significant difference between the biopsies from the biceps brachii and vastus lateralis. In the vastus lateralis, there was a reduction in fast-twitch fiber areas, which were smaller than in the biceps brachii (not studied at the previous investigation). There were also more histopathologic changes in the vastus lateralis than in the biceps brachii. The enzymatic activities of lactate dehydrogenase and myokinase, which were studied on both occasions in the vastus lateralis, did not change, and the activities of the other measured enzymes indicated a maintained metabolic capacity at high age. Oxidative enzymatic activities were higher in the vastus lateralis, and glycolytic enzymatic activities were higher in the biceps brachii, which could partly be explained by differences in relative fiber areas.
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PMID:Muscle morphology, enzymatic activity, and muscle strength in elderly men: a follow-up study. 376 79

Use was made of mitochondria isolated from heart left ventricles of either spontaneously hypertensive or age-matched Wistar-Kyoto rats used as a control to find out whether hypertrophy (5-week-old rats) or hypertrophy/hypertension (24-week-old rats) can cause change in the mechanisms by which ATP is synthesised via ATP synthase and subsequently exported via the ADP/ATP translocator outside mitochondria. To do this, photometric measurements were made of the rate of ATP appearance in the extramitochondrial phase, which occurs as a result of ADP addition to mitochondria. In mitochondria from spontaneously hypertensive rats deficit of ATP production was found dependent on changes in the KmADP and Vmax values of both the ADP/ATP translocator and the ATP synthase. The ADP/ATP translocator was found to determine the rate of ATP production outside mitochondria in all the tested samples. In an initial investigation carried out to ascertain how cell ATP deficit can be counterbalanced, an increase in both adenylate kinase and creatine kinase activities was found in both hypertrophy and hypertrophy/hypertension. A possible increase in anaerobic glycolysis was also suggested by the increased lactate dehydrogenase activity.
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PMID:ATP synthesis and export in heart left ventricle mitochondria from spontaneously hypertensive rat. 985 86

Both platelet aggregation and high blood pressure are associated with development of atherosclerosis. Among other factors that modulate platelet aggregation and blood pressure, extracellular purines (e-purines) influence these processes via purinoceptors P1 and P2 for which they are natural ligands. We hypothesized that ecto-enzymes such as nucleoside triphosphate diphosphohydrolases (NTPDases), adenylate kinase, 5'-nucleotidase, and adenosine deaminase that regulate the level of e-purines may be involved in the development of atherosclerosis. The enzymatic assays were performed either on the fragments of human abdominal aortas obtained after death or on abdominal aneurysm samples collected during surgery. The substrates and products such as adenine nucleosides and nucleotides were analyzed using reverse phase high-performance liquid chromatography (HPLC) method. Here, we estimated and demonstrated the activities of these ecto-enzymes in the patients with atherosclerosis or atherosclerosis-like diseases such as abdominal aneurysm, myocardial infarction, or Leriche syndrome (LS) with worse thrombosis of extremities. In particular, we noticed reduction in activity of NTPDase1(app), NTPDase2(app), ecto-adenylate kinase( app), and ecto-adenosine deaminase(app); however, ecto-5'-nucleotidase(app) that hydrolyzed e-adenosine monophosphate (e-AMP) into e-adenosine did not show any significant changes. This led us to suggest that alteration of the activity of examined ecto-enzymes is responsible for the development of atherosclerosis or atherosclerosis-like diseases.
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PMID:Extracellular purine metabolism in blood vessels (Part II): Activity of ecto-enzymes in blood vessels of patients with abdominal aortic aneurysm. 2046 Mar 46