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)

Hyperhomocyst(e)inemia is associated with an increased risk of coronary artery disease and myocardial infarction. Both genetic and environmental factors influence the plasma level of homocysteine. One of the metabolic pathways for homocysteine involves the enzyme methylenetetrahydrofolate reductase (MTHFR), which regulates the conversion of homocysteine to methionine. A thermolabile variant of MTHFR is associated with reduced enzyme activity and increased plasma homocysteine levels. Recently, the cause of this variant of MTFHR has been identified as a single base change altering an alanine to a valine residue in the protein. Using a PCR-based assay to distinguish the normal and thermolabile variants of MTHFR in this study, we investigated whether the thermolabile variant is a genetic risk factor for myocardial infarction. In a study of 532 subjects (310 myocardial infarction patients and 222 population-based controls), we found no difference in either MTHFR genotype distribution (p = 0.57) or allele frequencies (p = 0.68) between cases and controls. The allele frequencies of the thermolabile variant were 0.34 and 0.35 in cases and controls, respectively. The age- and sex-stratified odds ratio for risk of myocardial infarction associated with homozygosity for the thermolabile variant was 0.85 (95% CI 0.50-1.50, p = 0.57) and that with carriage of the thermolabile allele was 1.06 (95% CI 0.73-1.52, p = 0.76). The odds ratios remained non-significant when restricted to young subjects (< 60 years) or males, and were not influenced by several other risk factors for myocardial infarction considered either singly or in combination. Interestingly, in both cases and controls, there was a trend toward a higher prevalence of hypertension in subjects carrying the normal allele, although as this is a post-hoc finding it needs to be interpreted with caution. The thermolabile variant of MTHFR is not a major risk factor for myocardial infarction and is unlikely to explain a significant proportion of the reported association of hyperhomocyst(e)inemia with coronary artery disease.
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PMID:Genetic analysis of thermolabile methylenetetrahydrofolate reductase as a risk factor for myocardial infarction. 875 47

Out of 12 patients with primary hyperlipidemia (HL) included in the study ischemic heart disease was diagnosed in 4 and hypertension stage I-II in 6 patients. HL stage II B, III, IV and V was registered in 7, 2, 2 and 1 patients, respectively. Hypolipidemic therapy included hypolipidemic diet and Lipanor (Sanofi-Chinoin-Winthrop, France) in a dose 100 mg once a day after evening meal. The course lasted 3 months. Blood serum was examined for concentrations of total cholesterol (CS), triglycerides (TG), CS of HDLP, glucose, uric acid, prothrombin, fibrinogen, alanine and asparagine transaminase, alkaline phosphatase, creatinine, total bilirubin. After 1 month of lipanol treatment mean total CS concentration in the serum fell by 21.9% and remained such for 2-3 months of treatment. 1 month after the drug discontinuation mean concentration of total CS was under the initial one by 4.65%. Mean serum concentrations of TG 1 month after treatment decreased by 41.7%, after 2 months by 48.8%. Mean concentration of HDLP CS after 1 month of treatment rose by 19.2% and by 33.1% after one more month. 1 month after Lipanor discontinuation mean HDLP CS concentration exceeded the baseline level by 16%. Fibrinogen and prothrombin index declined. Hypolipidemic effect of Lipanor varied from case to case.
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PMID:[A trial of the use of the hypolipidemic preparation Lipanor (ciprofibrate) in patients with primary hyperlipidemia]. 877 89

Losartan represent a novel approach in the treatment of hypertension. Clinical trials have reported a very low incidence of side effects. We describe two patients who developed increases in alanine/aspartate amino transferase of 8 and 15 times the upper normal limit, as well as thoracic pain, after a short time of treatment with losartan. The increase resolved after discontinuing losartan treatment.
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PMID:Marked hepatotoxicity associated with losartan treatment. 879 Sep 30

We tested several peptides related to des-Arg9-bradykinin as stimulants or inhibitors of B1 (rabbit aorta, human umbilical vein) and B2 (rabbit jugular vein, guinea pig ileum, human umbilical vein) receptors. We also incubated the compounds with purified angiotensin-converting enzyme from rabbit lung to test their resistance to degradation. We evaluated apparent affinities (in terms of the affinity constant pA2) of compounds and their potential residual agonistic activities (alpha E). Bradykinin and des-Arg9-bradykinin were used as agonists for the B2 and B1 receptors, respectively. Degradation of peptides by the angiotensin-converting enzyme was prevented in the presence of a D-residue in position 7 of des-Arg9-bradykinin. Replacement of Pro7 with D-Tic combined with Leu, Ile, Ala, or D-Tic in position 8 led to weak B1 receptor antagonists, some of which had strong residual agonistic activities on the B2 receptor preparations. The use of D-beta Nal in position 7, combined with Ile in position 8 and AcLys at the N-terminal (eg, AcLys[D-beta Nal7, Ile8]des-Arg9-bradykinin) gave the most active B1 receptor antagonist (pA2 of 8.5 on rabbit aorta and human umbilical vein), which is also partially resistant to enzymatic degradation. Extension of the N-terminal end by Sar-Tyr-epsilon Ahx (used for labeling purposes) and even cold-labeling of Tyr with iodine were compatible with high, selective, and specific antagonism of the B1 receptors. We compared some compounds with some already known B1 receptor antagonists to underline the novelty of new peptidic compounds.
Hypertension 1996 Nov
PMID:Structure-activity studies of B1 receptor-related peptides. Antagonists. 890 31

A 45-year-old man was hospitalized because of acute hepatitis. His serum cholinesterase (ChE) was below 10 IU/l (normal range: 105-240 IU/l) during the disease course and after his recovery. The patient was suspected of having familial hypocholinesterasemia. His family members were healthy except that his father had hypertension and gall stones. Analysis of ChE gene in the propositus and his family revealed three point mutations at nucleotides 298 (CCA to TCA), 1,410 (CGT to CGG) and 1,615 (GCA to ACA). The first mutation caused an amino acid change at codon 100 from proline to serine, which was a new mutation not previously reported, but the second one was a silent mutation. The third mutation resulted in an amino acid alteration from alanine to threonine at codon 539 in exon 4 of the ChE gene. The mode of transmission of these mutations is described.
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PMID:Familial hypocholinesterasemia found in a family and a new confirmed mutation. 905 91

Sixty two samples of amniotic fluid were submitted to biochemical investigation including 31 samples from women with pregnancy complicated by hypertension (studied group with blood pressure -65 +/- 15/95 +/- 5 mm Hg) and 31 samples deriving from healthy pregnant women (control group with mean blood pressure 118 +/- 10/74 +/- +/- 9 mm Hg). The following parameters of amniotic fluid were measured: 1) aminotransferases: alanine AlAT and aspartate AspAT, 2) alkaline phosphatase (APt) and its thermostable isoenzyme (APh), 3) ceruloplasmin (Crlp), 4) alpha-amylase (alpha-Amy). The study showed pregnancy complicated by hypertension is related to fetal salivary gland's immaturity presenting decreased activity of alpha amylase in amniotic fluid. Amniotic fluids deriving from women with pregnancy complicated by hypertension showed normal activities of AlAT, AspAT, APt, APh and Crlp.
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PMID:[Evaluation of fetal condition in pregnancy complicated by hypertension--biochemical assessment of amniotic fluid. II. Enzymes]. 928 52

High serum cholesterol and LDL-cholesterol level and high blood pressure are risk factors for cardiovascular disease (CVD). CVD risk factors usually occur simultaneously, fact that enhance personal and population CVD risk. Data from interventional studies suggest that reducing CAD risk factors significantly lowered risk of CAD. Fluvastatin, a statine, has been used in hypercholesterolemic populations. We report on a clinical trial (random selection) of fluvastatin vs. placebo on hipercholesterolemic patients (total cholesterol > or = 240 mg/dl and/or low-density lipoprotein cholesterol (LDL-C) > or = 160 mg/dl) on treatment of mild to moderate high blood pressure. Forty Latin-American patients were randomized to placebo or 40 mg per day for 8 weeks of fluvastatin. Fluvastatin patients had a clinical and statistical significant reduction on total cholesterol (27.7%) and LDL-C (39.1%) Vs a non-significant reduction on the placebo group (6.9% total cholesterol and 9.1% LDL-C). One patient had elevated aspartate (AST) and alanine (ALT) aminotransferases (three times the local laboratory upper normal levels) associated with a chronic alcohol consumption, reverted 6 weeks after protocol completion. There was no important secondary effects; also there was no differences on this regard between placebo and verum group. Fluvastatin proved to be safe and well tolerated for this group of patients under a wide range of high blood pressure treatment.
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PMID:[Clinical trial with sodium fluvastatin in patients with hypercholesterolemia associated with mild and moderate essential arterial hypertension]. 929 41

Taste preferences are altered to reflect physiological needs and to support the recovery from nutritional disorders. The central mechanism both recognition for and adaptation to a deficient essential nutrient, i.e. L-lysine, have been unveiled that the feeding center in the hypothalamus is a primary center nucleus to induce a neuronal plasticity responding to dietary intake of deficient nutrient in the brain and peripherally, such as sense of taste and its concentration change. Changing preferences may act as an alarm, signaling protein malnutrition or metabolic adult disease, such as hypertension for saltiness, diabetes for sweetness, etc. In addition, our consumption of alcohol beverage is still increasing despite of one of candidate to induce the hepatic disorders, because pharmacological function of alcohol in the brain is welcome for people enjoying meal or being relieved from stresses. Preference for both L-alanine and L-glutamine was observed when alcoholic rats fell in the hepatic disorder. Acute alcohol loading induced suppression of motor activity and the hepatic dysfunction, but both amino acids did obviously protect these alcoholic symptoms. People should have to require a little bit more specific L-amino acid physiologically and pharmacologically depending upon different states among aging, lifestyle, metabolic diseases and various stresses.
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PMID:[A new pharmacological and physiological aspects of L-amino acids]. 950 1

Deoxycorticosterone acetate (DOCA)-salt-treated rats developed marked hypertension after 4 weeks with an increase in aortic endothelin-1. Treatment of DOCA-salt hypertensive rats with a proteasome inhibitor, N-benzyloxycarbonyl-Ile-Glu(O-t-Bu)-Ala-leucinal, significantly reduced the elevation in systolic blood pressure and the effect was accompanied by a decrease in aortic endothelin- content. Thus, a proteasome-dependent proteolytic pathway appears to play an important role in the enhanced production of endothelin-1 in blood vessels and the consequent increase in blood pressure in this model of hypertension.
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PMID:A proteasome inhibitor lessens the increased aortic endothelin-1 content in deoxycorticosterone acetate-salt hypertensive rats. 968 28

A point mutation which caused a silent phenotype of human serum butyrylcholinesterase (BChE) was identified in the DNA of a 47-year-old Japanese woman who visited our hospital complaining of hypertension. The propositus exhibited an unusually low level of BChE activity, whereas her younger sister and her daughter had intermediate levels of BChE activity and her elder sister a normal level. Immunologically, the amount of BChE protein in the serum of the propositus was normal. DNA sequence analysis of the propositus identified a point mutation at codon 199 (GCA --> GTA), resulting in a Ala --> Val substitution. This alteration is one downstream codon from the catalytic active site (Ser, 198). A family study showed her younger sister and her daughter to have the same mutation.
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PMID:Identification of a point mutation associated with a silent phenotype of human serum butyrylcholinesterase--a case of familial cholinesterasemia. 969 84


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