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)

The aim of the study was the estimation of the lipid profile and prevalence of dyslipoproteinemia in patients with essential hypertension. The study group consisted of 108 outpatients (61 men and 47 women) with mild to moderate hypertension (HT), aged 35-64, who did not receive antihypertensive drugs for at least four weeks. The matched controls (MC) were randomly chosen for each HT patient from population of Warsaw inhabitants, covered by Pol-MONICA II screen. The concentrations of total cholesterol (CH) and triglycerides (TG) in serum and cholesterol in lipoprotein fractions and subfractions (LDL, HDL, HDL3) were measured by enzymatic methods. The levels of apolipoproteins (Apo A-I, Apo B) were estimated by immunoassay. Laboratory was under control of WHO-Lipid Reference Laboratory and CDC-NHLBI Lipid Standardization Program. In HT the concentration of cholesterol in LDL was significantly higher (p < 0.001) than in MC, both in men (by 15%) and in women (by 22%), but the concentrations of cholesterol in HDL and HDL3 and Apo A-I (in men only) were significantly lower (p < 0.001) in HT than in MC in men (by 21% and by 26%) as well in women (by 16% and by 25%). Also in HT group the mean levels of TG, CH and Apo B were higher than in MC, but these differences were significant only in TG level in men. In HT group the prevalence of normolipemia was twice lower than in MC (22% and 42%). Essential hypertension fractions is associated with abnormal levels of some lipoprotein fraction and with higher prevalence of hyperlipoproteinemia. The coexistence of both abnormalities may be particularly detrimental as important factor in the development of atherosclerosis.
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PMID:[Dyslipoproteinemia in primary hypertension]. 931 61

Two substrains of the fawn-hooded (FH) rat have been developed, one of which develops progressive hypertension and proteinuria, the FHH, and one which shows little increase in blood pressure and no renal damage, the FHL. Other hypertensive rodent models show primary metabolic disturbances before the development of renal damage, notably hypertriglyceridemia, which may also contribute to progression of renal disease. In this study we evaluated whether hyperlipidemia is a primary disturbance in FHH, or only occurs secondary to proteinuria. Lipid levels were determined before and after development of proteinuria, and compared to those found in age-matched FHL. We also determined whether reducing proteinuria with lisinopril would normalize lipid levels in aging FHH. At 4 weeks of age, proteinuria was very low (2-3 mg/day) in both FHH and FHL. While proteinuria increased steadily in aging FHH, reaching 350 +/- 62 mg/day at 40 weeks, much less increase was observed in FHL over the same period (32 +/- 5 mg/day at 40 weeks). Blood pressure was markedly higher in adult FHH than in FHL (158 +/- 2 vs. 129 +/- 2 mm Hg, p < 0.01). In 4-week-old FHL and FHH, plasma cholesterol levels were similar. Subsequently, cholesterol increased in FHH, reaching 3.4 +/- 0.9 mmol/l at 40 weeks, whereas cholesterol was barely affected by aging in FHL (2.1 +/- 0.2 mmol/l at 40 weeks). At 4 weeks, triglyceride levels were lowest in FHH. Subsequently, triglycerides increased in FHH, reaching 3.5 +/- 1.5 mmol/l at 40 weeks, as compared to 1.3 +/- 0.2 mmol/l in FHL. Besides a transient increase in triglyerides in lisinopril-treated FHH at 11 weeks, increments in blood pressure, proteinuria, cholesterol, triglycerides and apolipoproteins A-I, B and E aging FHH were effectively prevented by lisinopril. These data strongly suggest that there is no primary difference in lipid metabolism between FHH and FHL and that changes in plasma lipids in FHH as compared to FHL are all secondary to proteinuria.
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PMID:Hyperlipidemia is secondary to proteinuria and is completely normalized by angiotensin-converting enzyme inhibition in hypertensive fawn-hooded rats. 937 31

DNA polymorphisms in genes encoding apolipoproteins (apo) A-I, C-III, B and E and angiotensin-converting enzyme (ACE) have been proposed to be associated with the risk of coronary artery disease (CAD). We studied whether the same genetic markers would also be associated with the occurrence and extent of atherosclerosis in cervical arteries. DNA samples from 234 survivors of stroke or a transient ischaemic attack aged 60 years or less were examined. The presence of atherosclerosis was assessed using aortic arch angiograms. The SstI polymorphism of apoA-I/C-III gene locus, the XbaI polymorphism of apoB gene, common apoE phenotypes and the insertion/deletion polymorphism of the ACE gene were analysed. The allele frequencies of the apoA-I/C-III, apoB, apoE or ACE gene did not differ between the groups with (n = 148) or without (n = 85) cervical atherosclerosis. However, when patients with at least one apoE4 allele and one X2 allele of apoB were combined and compared with those without either of them (E2E3 or E3E3 and X1X1), a significant association with the presence of cervical atherosclerosis was found (P = 0.03). The patients having the E2E3 phenotype had a significantly elevated serum triglyceride level compared with those with the E3E3 phenotype (P = 0.03). Serum high-density lipoprotein (HDL) cholesterol was lower in the patients with the E2E3 phenotype than in those with the E3E3 and E3E4 (P = 0.01 and P = 0.06, respectively). The apoB or ACE genotypes were not significantly associated with serum lipid or lipoprotein levels. There was no association between the ACE gene polymorphism and the occurrence of hypertension. In conclusion, the interaction of common apoB and apoE alleles may increase the risk of atherosclerosis in cervical arteries.
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PMID:Genetic risk factors and ischaemic cerebrovascular disease: role of common variation of the genes encoding apolipoproteins and angiotensin-converting enzyme. 966 3

The present study was designed to examine blood pressure response to nitric oxide synthase-pathway inhibition and stimulation in normotensive and hypertensive diabetic rats. Rats treated with streptozotocin (60 mg/Kg i.p.) developed high blood glucose, polyuria and slow weight gain compared with control. One group of diabetic rats developed hypertension, consequently we studied three experimental groups: control rats (C), normotensive diabetic rats (ND) and hypertensive diabetic rats (HD). Mean arterial pressure (MAP), systolic blood pressure, diastolic blood pressure and heart rate were recorded: baseline time, 30 after L-nitro arginine methyl ester (L-NAME: 1 mg/Kg i.v.) and post L-arginine (L-arg: 250 mg/Kg i.v.) injection. L-NAME induced a significantly increase in MAP in all groups. This enhancement was smaller in diabetic than in control rats. The increase in MAP in HD was significantly lower than that in ND L-arg induced a significantly decrease in MAP in all groups. This decrease was significantly attenuated in diabetic compared with control rats. The degree of hypotension in response to L-arg in diabetic groups was lower in hypertensive than that in normotensive diabetic rats. These data suggest that an impairment of nitric oxide formation could be involved in the development of hypertension in this model.
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PMID:Effects of L-NAME and L-Arg on arterial blood pressure in normotensive and hypertensive streptozotocin diabetic rats. 969 76

Adhesion molecules on the endothelial cell membrane play an important role in the pathogenesis of atherosclerosis. Levels of soluble forms of cell adhesion molecules are reportedly elevated in patients with peripheral artery vessel disease and in patients with an atherosclerotic aorta. The present study investigated the association of serum levels of soluble vascular cell adhesion molecule 1 (sVCAM-1), soluble intercellular adhesion molecule 1 (sICAM-1), and soluble P-selectin (sP-selectin) with coronary heart disease (CHD) and the extent of coronary atherosclerosis, and examined the influence of serum levels of lipids, lipoproteins and apolipoproteins (apo) in subjects with (n=52, M/F:43/9) and without (controls, n=40, M/F:25/15) angiographically proven coronary atherosclerosis. After controlling for age and gender, levels of sVCAM-1 (least squares mean +/- std error: 565+/-36 ng/ml vs 540+/-41 ng/ml, ns), sICAM-1 (261+/-17ng/ml vs 247+/-19ng/ml, ns), and sP-selectin (142+/-8ng/ml vs 149+/-10 ng/ml, ns) in patients with coronary atherosclerosis were not different from those in controls, as assessed by an analysis of covariance. After also adjusting for body mass index, hypertension, diabetes mellitus, and smoking by a multiple logistic function analysis, the association of sVCAM-1, sICAM-1, and sP-selectin with CHD was still not significant. Levels of sVCAM-1, sICAM-1, and sP-selectin were also not related to the extent of coronary atherosclerosis as judged by the number of stenosed vessels. However, inverse (p<0.05) relationships were observed between sVCAMs and serum levels of HDL3-cholesterol, apo A-II, and lipoprotein containing apo A-I and A-II, between sICAMs and levels of apo A-II and Lp A-I/A-II (Lp A-I/A-II), and between sP-selectin and lipoprotein containing only apo A-I. In conclusion, serum levels of soluble VCAM-1, ICAM-1, and P-selectin were not related to CHD or the extent of coronary atherosclerosis, but were inversely related to serum levels of high-density lipoprotein-related lipoproteins.
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PMID:Levels of soluble cell adhesion molecules in patients with angiographically defined coronary atherosclerosis. 1008 83

This syndrome is a pathological entity of low incidence which mainly affects high density lipoprotein (HDL) metabolism. We here show the first case reported in our country, observed in a 63-year-old woman who showed bilateral corneal opacity and eruptive xanthomas in both arms. The lipoprotein profile disclosed severe hypertriglyceridemia and normocholesterolemia, although the percentage of cholesteryl esters was low. Plasma levels of HDL-cholesterol and HDL major apolipoproteins, A-I and A-II, were markedly decreased. The patient also showed glucose intolerance and hematological alterations related to abnormal lipid composition of erythrocyte membranes. As evaluated by the exogen substrate method, LCAT activity proved to be 82% lower in the patient than in a control subject. It is noteworthy that the patient had experienced cardiac events and presented hypertension, neither of which has been commonly documented in partial LCAT deficiency syndromes.
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PMID:[Partial lecithin-cholesterol acyltransferase (LCAT) deficiency syndrome]. 1034 28

Lipoprotein(a) (Lp(a)) is recognized as a new coronary risk factor, but few studies have quantitatively assessed the relationship of serum Lp(a) levels with other coronary risk factors in many patients undergoing coronary cineangiography. Seventeen coronary risk factors were quantified (i.e., age, gender, hypertension, impaired glucose tolerance, cerebrovascular accident, hyperuricemia, smoking, family history of ischemic heart disease (IHD), history of hyperlipidemia, Lp(a), total cholesterol, high density lipoprotein (HDL)-cholesterol, triglyceride, low density lipoprotein-cholesterol, apolipoproteins(apo)A-I,B, E) to determine their relationship with the numbers of involved coronary vessels using multiple regression test in 1,006 patients who underwent coronary cineangiogram (280 non-IHD patients: 144 men, 136 women; 726 IHD patients: 460 men, 266 women; age 16-84 years, mean 60.5+/-0.3). Multiple regression test indicated R = 0.506 and items that showed high beta weight and significant p level were age, Lp(a), impaired glucose tolerance, total cholesterol, cerebrovascular accidents, HDL-cholesterol, smoking, gender, family history of IHD, and apo-A-I (0.221, p<0.001; 0.174, p<0.001; 0.616, p<0.001; 0.138, p<0.001; 0.122, p<0.001; -0.12, p<0.001; 0.092, p<0.01; 0.091, p<0.01; 0.067, p<0.05; -0.065, p<0.05; respectively). It was concluded that Lp(a) is an independent, potential, and modifiable coronary risk factor, and that reduction of serum Lp(a) is important in the clinical management of patients with IHD.
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PMID:Lipoprotein(a) is a potential coronary risk factor. 1065 Dec 7

The present study was designed, first to investigate aortic arginase activity during the development and the establishment of mineralocorticoid-salt (DOCA-salt) hypertension, and second, to determine the relationship between arginase activity and blood pressure by giving a protein-supplemented diet (50% casein) known to increase hepatic arginase activity. Our results showed that aortic arginase activity in established hypertension of DOCA-salt rats was higher than in normotensive rats. The protein-supplemented diet (50% casein) accelerated the development of DOCA-salt hypertension. There was a positive correlation between arginase activity and the level of blood pressure in these DOCA-salt hypertensive rats fed 50% casein but not in DOCA-salt hypertensive rats on a normal (20% casein) diet. In normotensive rats, the protein-supplemented diet decreased aortic arginase activity and produced no change in systolic blood pressure. Our data suggest that aortic arginase activity is modified in established DOCA-salt hypertension and could participate in the physiopathology of arterial hypertension.
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PMID:Increased arginase activity in aorta of mineralocorticoid-salt hypertensive rats. 1068 26

In normotensive rats (NTR) and spontaneously hypertensive rats (SHR) with high (subgroup 1) and low (subgroup 2) level of the systemic arterial pressure (SAP) we studied an activity of arginase and nitric oxide synthase (NOS) in different tissues, and the content of their metabolites: urea and nitrit anion (NO2-). In isolated preparations of a thoracic aorta we recorded endothelium-dependent (ED) dilator reactions on acetylcholine (Ach). It has been found that in heart, aorta, plasma and erythrocytes of rats (subgroup 2) both the activity of arginase and content of urea increase remarkably. In heart, the activity of arginase reaches 27.96 +/- 5.92 nmol.min-1.mg-1 of protein, in aorta 4.74 +/- 0.99 nmol.min-1.mg-1 of protein (as compared with NTR 1.32 +/- 0.12 nmol.min-1.mg-1 of protein and 1.12 +/- 0.07 nmol.min-1.mg-1 of protein, accordingly). Content of urea in heart reaches 679.5 +/- 121.19 nmol.mg-1 of protein, in aorta 350.6 +/- 63.6 nmol.mg-1 of protein (in NTR it was 36.8 +/- 5.3 nmol.mg-1 of protein and 43.02 +/- +/- 9.55 nmol.min-1.mg-1 of protein, accordingly). It was followed with a decrease in the NOS activity and heterogeneous changes in NO2- content in the tissues under exploration. For example, the activity of NOS in heart and aorta decreased to 0.018 +/- 0.005 nmol.min-1.mg-1 of protein, in aorta 0.183 +/- 0.037 nmol.min-1.mg-1 of protein, accordingly, as compared to 0.093 +/- 0.014 nmol.min-1.mg-1 of protein and 0.41 +/- 0.07 nmol.min-1.mg-1 of protein in NTR. Content of NO2- in aorta decreased by 0.79 +/- 0.06 nmol.mg-1 of protein, but in heart it increased to 0.63 +/- +/- 0.13 nmol.mg-1 of protein, (in NTR it was 2.15 +/- 0.18 nmol.mg-1 of protein and 0264 +/- 0.04 nmol.min-1.mg-1 of protein, accordingly). In rats, subgroup 2, ED dilator responses of the smooth muscle (SM) of the thoracic aorta were inhibited by Ach (10(-6) mol). Their amplitude reduced by almost twice, and a latency for their response became 4 times as much. All the changes in the biochemical parametres in heart, aorta, plasma and erythrocytes, and changes in contractile activity of vascular SM proved to be also characteristic for rats in subgroup 1, but they were less expressed quantitatively. Thus, for the first time we have studied an activity of two alternative pathways for the metabolism of L-arginine on the model of arterial hypertension. The data obtained evidence that at hypertension non-oxidative (arginase) pathway of L-arginine metabolism is activated, while the oxidative pathway (NOS) is inhibited. Changes in the balance between them are followed with an essential inhibition of ED vasodilator responses. All this give us the prove to think of the origin for the arterial pressure increase to be both genetically and quantitatively determined damages in the biochemical homeostasis and dependent on it endothelial regulation of vascular tone.
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PMID:[Disorders of endothelium-dependent vascular reactions and of the arginase and NO-synthase pathways of L-arginine metabolism in arterial hypertension]. 1105 80

Nitric oxide (NO) has been identified as an effective vascular relaxant. This study analyses the contribution of the precursor L-arginine (L-arg) by oral administration in two kidney-two clip hypertension in the rat (2K-2C). Two groups were studied: sham (SH, n=21) and hypertensive (HT, n=15). After 4 weeks of surgery, a group of rats remained as controls (SHc and HTc, respectively), while others were supplemented with L-arg (1.25 g/L) in drinking water (SHa and HTa) for 3 weeks. Blood pressure was significantly increased in 2K-2C rats but remained unchanged after L-arg treatment. Plasma nitrite/nitrate concentrations were not different among groups. The contractile response of aorta to KCl, serotonin and the protein kinase C (PKC) stimulant, phorbol 12,13-dibutyrate (PDBu) was also evaluated. Higher contractile responses to PDBu (p<0.001) and lower relaxation to acetylcholine (Ach 10(-6) M, p<0.05 and 10(-5)M, p<0.02) were observed in aortic rings of HTc vs SHc; L-arg supplementation significantly diminished tension development to all agonists (p<0.05) but failed to modify the lower relaxation to Ach in HTa. Thromboxane (TxA(2)) - synthesis in rings of HTc was higher than in SHc under basal conditions (p<0.05). In the groups with supplement of L-arg, PDBu significantly stimulated prostacyclin (PGI(2)) synthesis more in HTa rats than in SHa ones (p<0.05). To conclude: 1) L-arg fails to modify hypertension development in 2K-2C rats; and 2) L-arg exerts a beneficial effect on the vascular wall, by reducing contractility in rings from HTa rats; it also improved PGI(2) synthesis under PDBu stimulation. 3) greater PKC activation and TxA(2) production rather than lower NO availability might result in systemic hypertension in 2K-2C rats.
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PMID:Effect of oral L-arginine administration for three weeks in two kidney-two clip hypertensive rats. 1126 99


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