Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty-five patients with mild to moderate essential hypertension were randomly assigned to receive 10 to 40 mg of manidipine HCl or 15 to 60 mg of delapril daily for 12 months. In the manidipine-treated group were 13 women and 5 men (mean age, 48.2 years) and in the delapril-treated group 11 women and 11 men (mean age, 53.7 years). Blood samples were taken at baseline and after 6 and 12 months of treatment and again at 2 months after treatment discontinuation. Significant reductions in blood pressure were observed in both treatment groups. The reduction in diastolic blood pressure was significantly greater in the manidipine-treated patients than in the delapril-treated patients; no significant between-groups differences in systolic blood pressure were noted. Heart rate increased significantly in the manidipine group. No changes in serum levels of total cholesterol, triglycerides, and high-density and low-density lipoprotein cholesterol were noted during or after treatment. In the manidipine group, a small but significant decrease in apolipoprotein (apo) A-I and an increase in lipoprotein(a) were found at 6 months and a significant increase in apo A-II and apo E at 12 months; in the delapril group a significant decrease in apo A-I was found at 6 months. The results indicate that both manidipine and delapril are lipid-neutral antihypertensive drugs, since neither drug greatly affected serum lipid metabolism.
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PMID:Effects of manidipine and delapril on serum lipids, lipoproteins, and apolipoproteins in patients with mild to moderate essential hypertension: a randomized trial with one-year follow-up. 128 88

Lipoprotein(a) (Lp(a)) has been established as an important independent risk factor for the development of cardiovascular disease. Apolipoprotein(a), together with apo B-100 the apolipoprotein of Lp(a), is homologeous to plasminogen but lacks fibrinolytic capacity and appeared to interfere with fibrinolysis in in vitro and ex vivo experiments. We determined the correlations between Lp(a) and other blood lipids (serum cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides), coagulation parameters (fibrinogen, factor VII, factor VIII:C fibrin monomers, thrombin-antithrombin III) and fibrinolysis parameters (tissue plasminogen activator antigen, plasminogen activator inhibitor-1 and D-dimer) in 54 patients with essential hypertension, in 65 non-insulin-dependent diabetic patients and in 116 insulin-regulated diabetic patients. Signs of activated coagulation and increased reactive fibrinolysis were found in all three patient groups. In the hypertensive patients, Lp(a) was significantly correlated with LDL-cholesterol (r = 0.25, P = 0.04) and triglycerides (r = -0.30, P = 0.03), while in insulin-regulated diabetics, Lp(a) was also correlated with LDL-cholesterol (r = 0.20, P = 0.03). In the hypertensive patients and both diabetic groups there was no correlation of Lp(a) with coagulation or fibrinolysis parameters. These data show that Lp(a) concentrations are not related to coagulation or fibrinolysis parameters in hypertensive or diabetic patients and confirm the presence of an activated coagulation system in these patient groups.
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PMID:Low order correlations of lipoprotein(a) with other blood lipids and with coagulation and fibrinolysis parameters in hypertensive and diabetic patients. 138 33

The study objective was to determine the effects of monotherapy with clonidine and atenolol versus placebo on serum lipids, apolipoproteins, and blood pressure in patients with mild primary hypertension. The protocol comprised a double blind, randomized, placebo-controlled 5-month prospective study carried out in an outpatient general internal medicine clinic in a university medical center. There were 92 patients ages 18 to 70, with mild primary hypertension (sitting diastolic blood pressure of greater than 90 mm Hg and less than 105 mm Hg) without significant cardiac, renal, cerebrovascular, hepatic, neoplastic, or hematologic disorders. Patients with severe hyperlipidemia or peripheral vascular disease were also excluded. All factors known to effect serum lipids were held constant throughout the study (i.e., diet, weight, exercise, caffeine, tobacco). Atenolol and clonidine significantly reduced blood pressure when compared with placebo. Atenolol caused significant increases in serum triglycerides and apolipoprotein B (p less than 0.05) and significant reductions in high-density lipoprotein-cholesterol, apolipoproteins A-I and A-II (p less than 0.05). Atenolol also induced a significant adverse effect on all lipid ratios, increasing total cholesterol/high density lipoprotein-cholesterol, low density lipoprotein-cholesterol/high density lipoprotein-cholesterol, apolipoprotein B/apolipoprotein A-I and apolipoprotein B/apolipoprotein A-II ratios and decreasing low density lipoprotein-cholesterol/apolipoprotein-B ratio (p less than 0.05). Clonidine caused significant reductions in high-density lipoprotein-cholesterol, apolipoproteins AI and AII (p less than 0.05 but was neutral on all other lipids, lipid subfractions, and apolipoproteins. Clonidine did not significantly alter any of the lipid ratios.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of clonidine hydrochloride versus atenolol monotherapy on serum lipids, lipid subfractions, and apolipoproteins in mild hypertension. 219 93

We compared the effects of sustained-release diltiazem and captopril on blood pressure control and lipid profile. Forty-eight patients with primary hypertension were included in this randomized, double-blind, crossover study and 43 completed the trial. Following a two-to four-week placebo run-in period, each patient initially received either diltiazem (60-180 mg twice daily) or captopril (25-75 mg twice daily) for 16 weeks and then crossed over to the other drug after an interim placebo washout period. Both drugs significantly reduced systolic (SBP) and diastolic (DPB) blood pressure compared to baseline. However, supine (P less than 0.01), sitting and standing (P less than 0.05) DPB was lower with diltiazem than with captopril. Moreover, BP control (sitting DBP less than 90 mmHg) was achieved in a greater proportion of patients treated with diltiazem (63 vs 44%). Heart rate was significantly reduced (P less than 0.001) with diltiazem in all positions but was unchanged with captopril. Lipid, lipoprotein and apolipoprotein concentrations were not modified with either treatment. We conclude that both diltiazem and captopril are effective antihypertensive agents without deleterious effects on lipid metabolism. However diltiazem provides a better prolonged control of BP and may offer some advantages for patients in whom a slower heart rate would be beneficial.
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PMID:Comparative effects of diltiazem sustained-release and captopril on blood pressure control and plasma lipoproteins in primary hypertension: a randomized, double-blind, crossover study. 228 45

Nineteen patients with mild essential hypertension received 20 mg of arotinolol daily for 12 weeks. The patients' systolic and diastolic blood pressures and pulse rate decreased significantly after arotinolol. The ratio of apolipoprotein B to apolipoprotein A-I decreased significantly after treatment. No significant changes were observed in serum and lipoprotein lipid levels, apolipoprotein levels, or in the ratio of low-density lipoprotein cholesterol to high-density lipoprotein cholesterol. The results indicate that arotinolol is an effective antihypertensive agent with favorable effect on apolipoproteins.
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PMID:Effects of arotinolol on serum lipid and apolipoprotein levels in patients with mild essential hypertension. 247 85

The effect of the angiotensin converting enzyme inhibitor enalapril on serum lipids, apolipoproteins, and lipoproteins was studied in 21 patients with mild essential hypertension. The drug was administered at a dosage of 2.5 to 10 mg daily for 12 weeks. Enalapril significantly decreased the very low-density lipoprotein (VLDL) fraction at eight and 12 weeks. The apolipoprotein (apo) A-I and A-II fractions were significantly increased by 10% and 7.8%, respectively, at 12 weeks. The apo B fraction and the apo B/apo A-I ratio were significantly decreased at eight weeks (8% and 17%, respectively) and at 12 weeks (11% and 19%, respectively). Unchanged were the total cholesterol level, the lipoprotein cholesterol level, the triglyceride level, apo C-II, apo C-III, apo E, and the apo A-I/apo A-II ratio. This study confirmed that enalapril is an effective antihypertensive drug with a favorable effect on the lipid profile.
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PMID:Effects of enalapril on serum lipoproteins in mild essential hypertension. 254 8

Changes in serum lipids, apolipoproteins, and lipoproteins including high-density lipoprotein (HDL) subfractions following administration of captopril in patients with hypertension were studied. Captopril (25 mg twice daily) was administered over a 12-week period to 17 patients with mild to moderate essential hypertension. Captopril was observed to significantly reduce both systolic and diastolic blood pressure, as well as to increase HDL2- cholesterol (HDL2-C) and to decrease HDL3-cholesterol (HDL3-C); however, no significant changes in total HDL-C were recognized. Total cholesterol, low-density lipoprotein cholesterol, triglyceride, apolipoprotein (apo) A-I, apo A-II, apo B, apo C-II, apo C-III, and apo E did not change significantly. It is suggested that captopril monotherapy produces a favorable effect on HDL subfractions.
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PMID:Effect of captopril on high-density lipoprotein subfractions in patients with mild to moderate essential hypertension. 265 2

The effects of bunazosin and propranolol administration on hypertension and serum levels of lipids, lipoproteins and apolipoproteins were studied in a controlled, randomized multicenter study. After a 4-week washout period, 48 patients with mild to moderate essential hypertension were randomly assigned to either the bunazosin or the propranolol group. Twenty-four were treated with bunazosin (1 to 3 mg t.i.d.) and 24 with propranolol (10 to 40 mg t.i.d.) for 12 weeks. Systolic and diastolic blood pressures decreased significantly in both groups. After 12 weeks of bunazosin treatment, significantly lowered apolipoprotein (apo) B and apo B/apo A-I ratio (p less than 0.05, in both cases) were observed, in contrast to no changes in the propranolol group. Although the changes were not significant, bunazosin tended to decrease the ratio of total cholesterol minus HDL cholesterol to HDL cholesterol. There were no significant changes in total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, apo A-I, apo A-II, apo C-II, apo C-III and apo E for either bunazosin or propranolol. The difference between the two drugs was significant for the apo B/apo A-I ratio (p less than 0.05). Bunazosin monotherapy was shown to be as effective in reducing blood pressure as propranolol. In addition, its favorable effects on lipoprotein metabolism seem to offer an additional advantage in mitigating coronary risk.
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PMID:Comparative effects of bunazosin and propranolol on serum lipids and apolipoproteins in patients with essential hypertension. 267 72

The type and degree of changes in the lipid transporting system of blood plasma and levels of hormonal provision of the regulatory processes in juvenile obesity of different degrees were under study. A single fat food loading was used to detect the precursors or latent forms of disorders in lipoprotein spectrum and their hormone regulators. A total of 35 obese patients aged 16 to 18 and 30 age-matched healthy youths were examined. Analysis of the baseline values showed increased levels of apolipoprotein B, cholesterol, triglycerides, insulin, and reduced levels of apolipoprotein A1, high-density lipoprotein cholesterol in obese youths vs. controls. A atherogenic pattern of changes in the lipoprotein and apolipoprotein spectra of the plasma obese youths was clearly seen under conditions of fat food loading, these changes being associated with disordered insulin reaction to intake if exogenous fat. The examinees suffering from obesity a varying degree, mainly from the abdominal variant, presented with a complex of interrelated metabolic disorders (hyperinsulinemia, insulin resistance, dyslipoproteinemias),--the metabolic X syndrome, this referring them to a group at risk of developing atherosclerosis, essential hypertension, diabetes mellitus irrespective of the degree of general obesity.
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PMID:[The lipid transport system and its hormonal regulators in youths suffering from obesity]. 774 31

Plasma lipids, lipoproteins, and apolipoproteins were assessed in three groups of Nigerians at increased risk for atherosclerotic heart disease. The three patient groups, diabetes mellitus (n = 15), essential hypertension (n = 12), and hypertensive-diabetes mellitus (n = 11), were compared with age-matched, apparently healthy controls (n = 14). In subjects with diabetes mellitus, triglyceride and its related apolipoproteins CIII and CIII:NonB were significantly higher than controls. High-density lipoprotein cholesterol (HDL-C) was significantly lower; its related ratios, total/HDL-C and low-density lipoprotein cholesterol (LDL-C)/HDL-C were significantly higher than those for controls. Subjects with hypertension and hypertensive-diabetes mellitus had significantly higher values than controls for those lipids and lipid fractions considered atherogenic (total cholesterol, LDL-C, triglyceride, and the total/HDL-C and LDL-C/HDL-C ratios) as well as apolipoproteins B, CIII, and lipoprotein particles Lp(a) and CIII:NonB. Only hypertensive-diabetes mellitus subjects had lower HDL-C levels, while hypertension patients had significantly higher apolipoprotein AI and LpAI concentrations than controls. Subjects with hypertensive-diabetes mellitus had significantly worse lipid, lipoprotein, and apolipoprotein profiles both in terms of increased atherogenic and reduced anti-atherogenic parameters compared with subjects with diabetes mellitus or hypertension only. These studies suggest that Nigerians with diabetes, hypertension, and especially both hypertension and diabetes need to be fully evaluated from a lipid and lipoprotein standpoint, and any abnormalities detected need to be taken into consideration during therapy of this group of high-risk patients.
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PMID:Plasma lipids, lipoproteins, and apolipoproteins in Nigerian diabetes mellitus, essential hypertension, and hypertensive-diabetic patients. 789 82


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