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)

This paper covers the use of a long-term, ambulatory, indirect blood pressure monitoring device in a series of sequentially selected, consenting patients exhibiting an office blood pressure of 140/90 mmGh or greater. Of the 62 patients reported, 32 percent were found to have randomly elevated pressures neither requiring treatment or labeling as hypertensive. The Pressurometer III (Del Mar Avionics) offers a major improvement in the diagnosis of hypertension.
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PMID:Diagnostic use of ambulary blood pressure monitoring in medical practice. 725 36

We have the opportunity to evaluate a portable ambulatory device for the recording of sequential indirect arterial blood pressure and continuous electrocardiogram (Del Mar Avionics automatic ambulatory blood pressure recording device). With careful attention to technique, only 11% of systolic and 5% of diastolic blood pressure readings differed by more than 10 mm Hg as compared with a trained technician's observations simultaneously in the same arm. The device has been useful in the evaluation of borderline (labile) hypertension, hypertensive drug therapy programs, and various episodic cardiovascular phenomena--for example, vasodepressor syncope and pheochromocytoma crises.
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PMID:Evaluation of the Del Mar Avionics automatic ambulatory blood pressure-recording device. 731 1

This review has demonstrated that DN is common and can occur in one-third to one-half of IDDM patients. DN has a strong metabolic component, but there is also a component of genetic susceptibility. Persistent microalbuminuria is currently the most convenient and reliable predictor of nephropathy. Finally, Na/LiCTT, an experimental (and not yet commercially available) blood test, is felt to be a predictor of familial susceptibility to hypertension, and may be a marker of the risk of nephropathy in IDDM.
Del Med J 1995 Jul
PMID:Predicting renal disease in type I diabetics: smoke and fire or smoke and mirrors? 765 99

Intracranial hemorrhage is the third most frequent cause of cerebrovascular disease, but few genetic risk factors have been associated with its development. Recently, it has been reported that some polymorphisms that affect clotting factors increase the risk for thrombosis. However, reports have analyzed the effect of polymorphisms influencing the hemostatic state in bleeding disorders insufficiently. A case-control study was conducted of 201 patients with spontaneous intracranial hemorrhage and 201 control subjects matched for age, race, sex, and selected risk factors (hypertension, smoking, and alcohol consumption). Genomic polymerase chain reaction was used to analyze the prevalence of 4 polymorphisms: factor V Leiden, prothrombin 20210A, factor VII-323 Del/Ins of a decanucleotide, and factor XIII V34L. Subjects with factor V Leiden had decreased risk for spontaneous intracranial hemorrhage (odds ratio, 0.19; 95% confidence interval, 0.03-0.95). The frequency of the prothrombin 20210A/G genotype was also lower among patients than controls (1.5% vs 3%, respectively). Moreover, carriers of the -323 Ins allele of factor VII had a 1.54-fold risk for intracranial hemorrhage (95% CI, 1.03-2.72). Finally, no significant differences were observed in the prevalence of factor XIII V34L polymorphism between patients and controls. Therefore, new genetic factors affecting the risk for spontaneous intracranial hemorrhage were identified. These data, together with the relevance of these polymorphisms in thrombotic diseases, support the idea that a polymorphism may play opposite roles in thrombosis and hemorrhage, suggesting an explanation for the high frequency of these polymorphisms in the general population.
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PMID:Polymorphisms of clotting factors modify the risk for primary intracranial hemorrhage. 1169 36

Angiotensin-converting enzyme (ACE) activity is highly heritable and has been associated with cardiovascular disease. We are studying the effects of genes and environmental factors on hypertension and related phenotypes, such as ACE activity, in Mexican-American families. In the current study, we performed multipoint linkage analysis to search for quantitative trait loci (QTLs) that affect ACE activities on data from 793 individuals from 29 pedigrees from the San Antonio Family Heart Study. As expected, we obtained strong evidence (maximum log of the odds [LOD]=4.57, genomic P=0.003) that a QTL for ACE activity is located on chromosome 17 near the ACE structural locus. We subsequently performed linkage analyses conditional on the effect of this QTL and obtained strong evidence (LOD=3.34) for a second QTL on chromosome 4 near D4S1548. We next incorporated the ACEIns/Del genotypes in our analyses and removed the evidence for the chromosome 17 QTL (maximum LOD=0.60); however, we retained our evidence for the QTL on chromosome 4q. We conclude that the QTL on chromosome 17 is tightly linked to ACE and is in strong disequilibrium with the insertion/deletion polymorphism, which is consistent with other reports. We also have evidence that an additional QTL affects ACE activity. Identification of this additional QTL might lead to alternate means of prophylaxis.
Hypertension 2004 Feb
PMID:Two quantitative trait loci affect ACE activities in Mexican-Americans. 1470 62

The purpose of this study was to determine the degree of agreement among different frequencies of blood pressure measurements (FoM) in 24-hour ambulatory blood pressure monitoring (ABPM) in their ability to obtain useful clinical information. ABPM records were obtained with a Del Mar IV Avionics device from 49 hospitalised preeclamptic women with a FoM of 7 per hour (high-FoM). With these records, we simulated two sets of data as if measurements had been recorded at a rate of 1 measurement per hour (low-FoM) and of 2 per hour (medium-FoM). Diastolic blood pressure > 89 mmHg defined hypertension and > 109 mmHg, severe hypertension The median and 25th and 75th centiles for the differences in hypertensive rate detected (expressed as percentage points) between lowFoM vs. high-FoM was 0.00 (- 3.4-3.00) and between medium-FoM vs. high-FoM,- 1.04 (- 3.7-1.5). The agreement in the detection of severely affected patients was 85% (CI 95%: 74-96) between low-FoM and high-FoM and 87% (CI 95%: 77-98), between medium-FoM and high-FoM. Average blood pressure was similar in the three FoMs studied at day-time and night-time. We did not find any strong argument to perform ABPM at a high-FoM. Lower FoM are more comfortable for the patient and could reduce equipment deterioration, while providing equivalent information to that supplied by high-FoM.
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PMID:Agreement between different frequencies of measurements in ambulatory blood pressure monitoring. 1551 77

Associations of polymorphisms in the angiotensin I-converting enzyme (ACE), apolipoprotein B (APOB) and apolipoprotein E (APOE) genes with hypertension and variations in lipid serum levels were evaluated in 184 Afro-Brazilians with a familial history of coronary artery disease (CAD). ACE (Ins/Del) and APOB (Ins/Del, XbaI, and EcoRI) and APOE (HhaI) polymorphisms were determined by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) analyses on agarose, and polyacrylamide gel electrophoresis. Serum lipids were measured by means of routine enzymatic assays. The results showed a high frequency of hypertension (44%) in Afro-Brazilians that was increased in subjects >40 years old and those with a blood mass index (BMI) higher than 25 kg/m(2) (P<0.001). The ACE Del allele was associated with hypertension in men >40 years old (P<0.05). APOE (HhaI) and APOB (XbaI and Ins/Del) polymorphisms were not associated with hypertension or variations in serum concentrations of lipids, while subjects with the APOB E- allele had higher low-density lipoprotein cholesterol (LDL-C) levels than E+ carriers (P<0.05). These results suggest that ACE Ins/Del polymorphism is associated with hypertension, and APOB EcoRI polymorphism is associated with LDL-C variation in Afro-Brazilians.
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PMID:Five polymorphisms in gene candidates for cardiovascular disease in Afro-Brazilian individuals. 1554 63

17alpha-Hydroxylase deficiency is a rare disease caused by mutation of the CYP17 gene, resulting in hypertension, hypokalemia, female sexual infantilism or male pseudohermaphroditism, low blood cortisol and low plasma renin activity. Herein, we report a female Taiwanese with 17alpha-hydroxylase deficiency. The CYP17 genes of this patient and five members of her family were analyzed by PCR-direct sequencing. One allele of the patient contains a 9-bp (c. 1459-1467 GACTCTTTC: D487, S488, F489) deletion, which is prevalent in Southeast Asia. The other allele has a 6-bp (c. 1480-1485 AAGGTG: K494, V495) deletion and an R496L (c. 1487 G>T) missense mutation, which is a novel mutation. Site-directed mutagenesis, in vitro expression and functional analysis in HEK-293T cells showed that this novel mutation [K494_V495 Del; R496L] resulted in complete loss of 17alpha-hydroxylase and 17,20-lyase activity. Thus this novel mutation in the extreme C-terminus abolishes enzyme activity, and when accompanied by a 9-bp deletion at codons 487-489 in the other allele, results in 17alpha-hydroxylase/17,20-lyase deficiency in this patient.
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PMID:A novel compound heterozygous mutation of K494_V495 deletion plus R496L and D487_F489 deletion in extreme C-terminus of cytochrome P450c17 causes 17alpha-hydroxylase deficiency. 1648 11

Sequence variations in the human alpha2 adrenergic receptor genes (ADRA2A and ADRA2C) have been implicated as a cause of hypertension in blacks. Although certain alleles are selectively enriched in blacks, their association with hypertension is based on small convenience samples and has not been evaluated in larger populations. From a stratified random population sample of 3398 individuals (52% blacks), we obtained DNA samples together with an in-home health interview, 10 in-home measurements of blood pressure, and cardiac MRI. We tested for associations among hypertension, untreated blood pressure, and parameters of hypertensive heart disease with 2 alleles, a DraI restriction fragment length polymorphism in the ADRA2A gene and a deletion of residues 322 to 325 in the ADRA2C gene. Although both alleles were selectively enriched in this black population, we found no association of either allele with hypertension, untreated blood pressure, or any of the cardiac function parameters. In a logistic model that controlled for age, body mass index, diabetes, and smoking, the adjusted odds ratio (OR) for hypertension was 1.0 (95% CI, 0.8 to 1.2), and 1.0 (95% CI, 0.9 to 1.2) for ADRA2A and ADRA2C variant alleles. In subjects not receiving prescription blood pressure medication, neither of these alleles, alone or in combination, was predictive of blood pressure, heart rate, left ventricular mass, cardiac output, systemic vascular resistance, or aortic compliance. Both the DraI restriction fragment length polymorphism in ADRA2A and the ADRA2C (Del 322 to 325) can be excluded as major candidate alleles for hypertension in blacks.
Hypertension 2006 Jun
PMID:Do allelic variants in alpha2A and alpha2C adrenergic receptors predispose to hypertension in blacks? 1663

Vernonia amygdalina Del. (Family Compositae) is used in Nigerian folk medicine as a tonic and remedy against constipation, fever, high blood pressure, and many infectious diseases. We have evaluated the hepatoprotective and antioxidant effects of an aqueous extract of V. amygdalina leaves against acetaminophen-induced hepatotoxicity and oxidative stress in mice in vivo. Activities of liver marker enzymes in serum (glutamate-oxaloacetate transaminase, glutamate-pyruvate transaminase, lactate dehydrogenase, and alkaline phosphatase) and bilirubin levels were determined colorimetrically, while catalase activity, lipid peroxidation products, thiobarbituric acid-reactive substances (TBARS), iron, and total protein concentrations were measured in liver homogenate. Acetaminophen challenge (300 mg/kg, i.p) for 7 days caused significant (P < .01) increases in the levels of bilirubin, liver enzymes, TBARS, and iron, while catalase activity and total protein level were reduced significantly (P < .01). Preadministration of V. amygdalina resulted in a dose-dependent (50-100 mg/kg) reversal of acetaminophen-induced alterations of all the liver function parameters by 51.9-84.9%. Suppression of acetaminophen-induced lipid peroxidation and oxidative stress by the extract was also dose-dependent (50-100 mg/kg). The results of this study suggest that V. amygdalina elicits hepatoprotectivity through antioxidant activity on acetaminophen-induced hepatic damage in mice.
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PMID:Hepatoprotective and antioxidant activities of Vernonia amygdalina on acetaminophen-induced hepatic damage in mice. 1720 40


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