dihydropyridines and Hypercholesterolemia

dihydropyridines has been researched along with Hypercholesterolemia* in 11 studies

Trials

3 trial(s) available for dihydropyridines and Hypercholesterolemia

ArticleYear
[Hypotensive efficacy and tolerability of combination of dihydropyridine and non-dihydropyridine calcium antagonists in the treatment of patients with arterial hypertension].
    Kardiologiia, 2007, Volume: 47, Issue:11

    Topics: Adult; Calcium Channel Blockers; Diabetes Mellitus, Type 2; Dihydropyridines; Dose-Response Relationship, Drug; Drug Therapy, Combination; Female; Humans; Hypercholesterolemia; Hypertension; Hypertrophy, Left Ventricular; Male; Middle Aged; Nifedipine; Obesity; Treatment Outcome; Verapamil

2007
[Evaluation of lercanidipine in the general practice setting].
    Anales de medicina interna (Madrid, Spain : 1984), 2003, Volume: 20, Issue:6

    To determine the efficacy and tolerability of a long-acting dihydropyridine in the clinical settings of general practice.. 110 essential hypertensives were included (age 62.3 +/- 10.8 years, 51 men and 53 women, 38/ obese -IMC >30 kg/m2, ten diabetics). 104 patients ended the followup. Patients were treated with lercanidipine 10 mg once daily in the morning. Follow-up lasted 6 months. When blood pressure was not controlled (BP < 140/90 mmHg) in any visit, a second drug was added, excluding calcium channel blockers. Antiadrenergic drugs were recommended. If patients were not controlled ittwo consecutive visits they were excluded from follow-up.. Significant reductions in both systolic (baseline 157.4 +/- 11.7 vs 131.1 +/- 6.8 mmHg, p < 0,001) and diastolic BP (baseline 94.7 +/- 5.8 vs 80.0 +/- 5.5 mmHg, p < 0,001) were attained at six months. Mean SBP decrease was 26.7 mmHg and mean DBP reduction was 15.6 mmHg. At the study end, 84.3/ of the patients achieved a BP < 140/90 mmHg. Thirty patients needed a second drug to become controlled (26 at the study end). The overall incidence of adverse effects was 4,4/ (n=6) and just three patients withdrew the treatment due to untoward effects. Plasmatic cholesterol lowered from 225.3 +/- 41.0 to 216.7 +/- 25.3 mg/dl (p = 0,03) and urate decreased from 5.6 +/- 1.6 to 5.1 +/- 1.4 mgldl, p = 0,03).. Lercanidipine is a calcium channel blockers of high efficacy and low incidence of adverse effects in the clinical settings of general practice. It seems to have a positive metabolic effects on plasmatic levels of cholesterol and urate.

    Topics: Aged; Antihypertensive Agents; Calcium Channel Blockers; Calcium Channels, L-Type; Cholesterol; Diabetes Complications; Dihydropyridines; Family Practice; Female; Follow-Up Studies; Humans; Hypercholesterolemia; Hypertension; Male; Middle Aged; Obesity; Treatment Outcome; Uric Acid

2003
[Evaluation of psychosomatic symptomatology in hypertensive patients treated with lercanidipine (LERCAPSICO study)].
    Anales de medicina interna (Madrid, Spain : 1984), 2003, Volume: 20, Issue:6

    To value the grade of anxiety and psychosomatic semiology in hypertensive patients treated with lercanidipine and to analyse their evolution. A secondary objective is to carry out a pharmacovigilance study with lercanidipine.. Prospective multicentre observational 6 month study in primary hypertensive patients with SBP between 140-180 mm Hg and/or 90-110 mm Hg DBP. After a washout period of 10 days, treatment with 10 mg (1-0-0) lercanidipine is initiated. If BP is not controlled treatment with ramipril 2.5 mg/day is instaured. Clinical check-ups are carried periodically with measurements of BP, Heart Rate, objective valuation of tolerance to the drug and observance. At the initiation and end of the study biochemical check-ups are carried out, the level of anxiety is measured using the STAI questionnaire (Trait subscale) (Evaluation in decatipes 0-4 without ansiety 4-7 moderate ansiety, 7-10 high ansiety) and the psychosomatic profile with a questionnaire designed by this group. (Scale 0-18; 0 large semiology, 18 without semiology). Clinical tolerance to the drug is valued both subjectively and objectively.. On included 538 patients. On registred 54 drop out, with side effects (3.75/). Completed the study 484 (237 M, 247 F), 429 of them with Lercanidipine in monotherapy (88.6/). Mean age 60.9 +/- 10.7. Mean BMI 29.1 +/- 5. The grade of anxiety did not alter during the study passing from 4.6 +/- 1.7 at the beginning of the study to 4.5 +/- 1.7 at the end of the study (valuation in decatypes) (ns). The psychosomatic semiology changed favourably from 10.7 +/-4.2 to 12.5 +/- 3.7 (p<0.00005). The evolution according to sex is similar. The mean SBP decreased from 165.6 +/- 12.2 mm Hg to 137.9 +/- 10.4 mm Hg (p<0.00005) and the mean DBP decreased from 96.5 +/- 8.1 mm Hg to 81.0 +/- 6.1 mm Hg (p<0.00005). Clinical tolerance was very good. Biochemical parameters were modified substantially: initial cholesterolemia 227.7 mg/dl and final cholesterolemia 213.6 mg/dl (p<0.00005); initial glucose 108.4 mg/dl and final glucose 105.7 mg/dl (p<0.00005).. The mean level of anxiety in the group studied is confirmed not to vary during the length of the study. Psychosomatic semiology is reduced being statistically significant. Lercanidipine is shown to be very effective as antihypertensive and well tolerated. 164

    Topics: Adolescent; Adult; Aged; Aged, 80 and over; Antihypertensive Agents; Anxiety; Blood Glucose; Calcium Channel Blockers; Calcium Channels, L-Type; Cholesterol; Diabetes Complications; Diabetes Mellitus; Dihydropyridines; Female; Humans; Hypercholesterolemia; Hypertension; Male; Middle Aged; Prospective Studies; Psychophysiologic Disorders; Treatment Outcome

2003

Other Studies

8 other study(ies) available for dihydropyridines and Hypercholesterolemia

ArticleYear
A case of vasospastic angina showing resolution of coronary vasospasm in acetylcholine provocation test corresponding to regression of coronary atherosclerosis.
    International journal of cardiology, 2008, Mar-28, Volume: 125, Issue:1

    We experienced a case of vasospastic angina showing resolution of vasospasm in the acetylcholine provocation test corresponding to regression of coronary atherosclerotic plaque following treatment with a combination of benidipine and pravastatin.

    Topics: Acetylcholine; Angina Pectoris; Angina Pectoris, Variant; Anticholesteremic Agents; Cholinergic Agents; Coronary Artery Disease; Coronary Vasospasm; Dihydropyridines; Humans; Hypercholesterolemia; Male; Middle Aged; Pravastatin; Ultrasonography; Vasodilator Agents

2008
Comparison of the antiatherosclerotic effects of dihydropyridine calcium channel blocker and HMG-CoA reductase inhibitor on hypercholesterolemic rabbits.
    Vascular pharmacology, 2007, Volume: 46, Issue:4

    The antiatherosclerotic effects of the dihydropyridine-type calcium channel blocker, benidipine hydrochloride (benidipine), and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, pravastatin sodium (pravastatin), were compared in hypercholesterolemic rabbits. Male, New Zealand white rabbits were fed a 0.5% cholesterol diet. Pravastatin (10 mg/kg) or benidipine (10 mg/kg) was orally administered once daily after start of feeding. After 8 weeks of cholesterol feeding, serum cholesterol was increased and endothelial function of thoracic aorta was impaired. Pravastatin prevented elevation of serum cholesterol and aortic tunica intima hyperplasia. Although benidipine had little effect on serum cholesterol, it significantly inhibited aortic tunica intima hyperplasia and impairment of endothelial function. Expression levels of the vascular cell adhesion molecule-1 (VCAM-1) and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) mRNA in aorta of hypercholesterolemic rabbit were higher than those of normal rabbit. Benidipine significantly prevented upregulation of VCAM-1 mRNA expression and showed a tendency to inhibit elevation of LOX-1 mRNA expression. Pravastatin significantly prevented upregulation of both VCAM-1 and LOX-1 mRNA expression. The results demonstrate that pravastatin inhibits increase of serum cholesterol and vascular dysfunction in hypercholesterolemic rabbit. Benidipine is effective in preventing vascular hyperplasia without altering serum cholesterol levels and this may be due to inhibition of expression of VCAM-1.

    Topics: Animals; Aorta, Thoracic; Atherosclerosis; Calcium Channel Blockers; Cholesterol; Dihydropyridines; Disease Models, Animal; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypercholesterolemia; Hyperplasia; Male; Pravastatin; Rabbits; RNA, Messenger; Scavenger Receptors, Class E; Time Factors; Tunica Intima; Up-Regulation; Vascular Cell Adhesion Molecule-1; Vasodilation

2007
Increased NADH-oxidase-mediated superoxide production in the early stages of atherosclerosis: evidence for involvement of the renin-angiotensin system.
    Circulation, 1999, Apr-20, Volume: 99, Issue:15

    Angiotensin II activates NAD(P)H-dependent oxidases via AT1-receptor stimulation, the most important vascular source of superoxide (O2*-). The AT1 receptor is upregulated in vitro by low-density lipoprotein. The present study was designed to test whether hypercholesterolemia is associated with increased NAD(P)H-dependent vascular O2*- production and whether AT1-receptor blockade may inhibit this oxidase and in parallel improve endothelial dysfunction.. Vascular responses were determined by isometric tension studies, and relative rates of vascular O2*- production were determined by use of chemiluminescence with lucigenin, a cypridina luciferin analogue, and electron spin resonance studies. AT1-receptor mRNA was quantified by Northern analysis, and AT1-receptor density was measured by radioligand binding assays. Hypercholesterolemia was associated with impaired endothelium-dependent vasodilation and increased O2*- production in intact vessels. In vessel homogenates, we found a significant activation of NADH-driven O2*- production in both models of hyperlipidemia. Treatment of cholesterol-fed animals with the AT1-receptor antagonist Bay 10-6734 improved endothelial dysfunction, normalized vascular O2*- and NADH-oxidase activity, decreased macrophage infiltration, and reduced early plaque formation. In the setting of hypercholesterolemia, the aortic AT1 receptor mRNA was upregulated to 166+/-11%, accompanied by a comparable increase in AT1-receptor density.. Hypercholesterolemia is associated with AT1-receptor upregulation, endothelial dysfunction, and increased NADH-dependent vascular O2*- production. The improvement of endothelial dysfunction, inhibition of the oxidase, and reduction of early plaque formation by an AT1-receptor antagonist suggests a crucial role of angiotensin II-mediated O2*- production in the early stage of atherosclerosis.

    Topics: Acetylcholine; Acridines; Amlodipine; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Animals; Antihypertensive Agents; Arteriosclerosis; Diet, Atherogenic; Dihydropyridines; Electron Spin Resonance Spectroscopy; Hypercholesterolemia; Lipids; Luminescent Measurements; Macrophages; Male; Multienzyme Complexes; NADH, NADPH Oxidoreductases; Phenylephrine; Rabbits; Receptor, Angiotensin, Type 1; Receptor, Angiotensin, Type 2; Receptors, Angiotensin; Receptors, LDL; Renin-Angiotensin System; Superoxides; Tetrazoles; Up-Regulation; Vasoconstriction; Vasoconstrictor Agents; Vasodilation; Vasodilator Agents

1999
Effect of lercanidipine and its (R)-enantiomer on atherosclerotic lesions induced in hypercholesterolemic rabbits.
    British journal of pharmacology, 1998, Volume: 125, Issue:7

    The in vivo antiatherogenic activity of the calcium antagonist lercanidipine and its (R)-enantiomer was investigated in two different types of atherosclerotic lesions (hyperplastic and fatty-streak lesions) in rabbits. Lercanidipine (0.3, 1, and 3 mg kg(-1) week(-1)) as well as its (R)-enantiomer at 3 mg kg(-1) week(-1) were given by subcutaneous injection for 10 weeks to White New Zealand rabbits, with cholesterol feeding beginning at week 2. The hyperplastic lesion was obtained by positioning a hollow silastic collar around one carotid artery, while aortic fatty streak lesions were induced by cholesterol feeding. In untreated animals (n=5), 14 days after collar positioning an intimal hyperplasia was clearly detectable: the arteries without collar showed a intima/media (I/M) ratio of 0.03+/-0.02, whereas in carotids with a collar the ratio was 2+/-0.42. In lercanidipine-treated animals a significant and dose-dependent effect on intimal hyperplasia was observed. I/M ratios were 0.73+/-0.4, 0.42+/-0.1, 0.32+/-0.1 for 0.3, 1, and 3 mg kg(-1) week(-1), respectively (P<0.05). The lercanidipine enantiomer (3 mg kg(-1) week(-1)) was as effective as the racemate (0.41+/-0.11). Proliferation of smooth muscle cells, assessed by incorporation of BrdU into DNA, was reduced by about 50%, 70%, 85%, and 80% by lercanidipine (0.3, 1, and 3 mg kg(-1) week(-1)) and its (R)-enantiomer, respectively. The area of fatty-streaks in the aorta (n = 11-15) was significantly reduced by lercanidipine (3 mg kg(-1) week(-1), 16% vs 27%, P<0.05), a trend was observed also with lower doses. When different segments of the aorta were considered (arch, thoracic, abdominal) a significant and dose-dependent effect in the thoracic and abdominal aorta was observed also at lower doses. The (R)-enantiomer was as effective as lercanidipine. These results suggest a direct antiatherosclerotic effect of lercanidipine, independent of modulation of risk factors such as hypercholesterolemia and/or hypertension as demonstrated by the absence of stereoselectivity.

    Topics: Animals; Arteries; Arteriosclerosis; Calcium Channel Blockers; Cholesterol, Dietary; Dihydropyridines; Disease Models, Animal; Hypercholesterolemia; Hyperplasia; Macrophages; Male; Rabbits

1998
Action of elgodipine on atherosclerosis development, cell growth, and oncogene expression in vascular smooth muscle cells.
    General pharmacology, 1997, Volume: 28, Issue:3

    1. Elgodipine (ELG) had no significant effect on aortic content of cholesterol, plasma cholesterol, or triglycerides concentrations in cholesterol-fed rabbits. However, ELG administration produced a dose-dependent and significant reduction of calcium content of the aorta. 2. In vitro studies showed that ELG was able to inhibit vascular smooth muscle proliferation through a mechanism independent of the expression of the transcription factors c-fos and c-jun.

    Topics: Animals; Aorta, Thoracic; Arteriosclerosis; Blood Pressure; Calcium; Calcium Channel Blockers; Cell Division; Cells, Cultured; Cholesterol, Dietary; Dihydropyridines; Gene Expression; Hypercholesterolemia; Lipoproteins; Male; Muscle, Smooth, Vascular; Proto-Oncogene Proteins; Rabbits; Triglycerides

1997
Direct antiatherogenic activity of isradipine and lacidipine on neointimal lesions induced by perivascular manipulation in rabbits.
    Pharmacological research, 1997, Volume: 35, Issue:5

    The in vivo antiatherogenic activity of two calcium antagonists of the dihydropyridine class (isradipine and lacidipine) was investigated in a new experimental model. The proliferative lesion induced in the rabbit carotid artery was obtained by positioning a hollow silastic collar around the vessel. The neointimal formation was determined by measuring cross sectional thickness of intimal (I) and medial (M) tissue of fixed arteries obtained 14 days after collar placement. The effectiveness in inhibiting neointimal formation was assessed for isradipine (0.5, 1 and 4 mg kg-1 day-1) in normocholesterolemic (NC) animals and for lacidipine (1, 3, and 10 mg kg-1 day-1) in hypercholesterolemic (HC) rabbits. In NC control animals a neointimal formation was clearly detectable (I/M 0.53 +/- 0.18, n = 5). In isradipine-treated groups I/M ratios were significantly decreased (0.15 +/- 0.03, 0.12 +/- 0.02, 0.1 +/- 0.02 for the 0.5, 1 and 4 mg kg-1 day-1 doses respectively). In HC rabbits the administration of cholesterol 1% mixed with food and drug treatment started either 60 days before collar insertion (pretreated group, HC60) or on the same day (non pretreated group, HC15) of the collar placement. Only the pharmacological pretreatment was effective in reducing neointimal formation (0.47 +/- 0.02, 0.4 +/- 0.09, and 0.32 +/- 0.02 for dose 1, 3 and 10 mg kg-1 day-1 vs 1.1 +/- 0.14 in control animals). The inhibition of neointimal hyperplasia was much less evident in nonpretreated animals (0.7 +/- 0.15, 0.6 +/- 0.18 and 0.43 +/- 0.08 for dose 1, 3, and 10 mg kg-1 day-1 vs 0.72 +/- 0.2 in control animals). These results suggest a direct antiatherosclerotic effect of isradipine and lacidipine on neointimal hyperplasia induced in NC and HC pretreated rabbits independently of modulation of risk factors such as hypercholesterolemia and/or hypertension.

    Topics: Animals; Arteriosclerosis; Calcium Channel Blockers; Carotid Arteries; Dihydropyridines; Dose-Response Relationship, Drug; Hypercholesterolemia; Isradipine; Male; Muscle, Smooth, Vascular; Neovascularization, Pathologic; Rabbits

1997
Effect of lacidipine on fatty and proliferative lesions induced in hypercholesterolaemic rabbits.
    British journal of pharmacology, 1996, Volume: 118, Issue:2

    1. The in vivo antiatherogenic activity of the calcium antagonist, lacidipine, was investigated in two different types of atherosclerotic lesions (proliferative and fatty lesions) induced in rabbits. 2. The proliferative lesion was obtained by positioning a hollow silastic collar around one carotid artery, while aortic fatty lesions were induced by cholesterol feeding. Cholesterol (1%) and lacidipine (1, 3, and 10 mg kg-1) were given daily mixed with standard diet for 8 weeks to White New Zealand rabbits. The intimal hyperplasia (proliferative lesion) was induced 6 weeks after dietary and drug treatment started. 3. The neointimal formation was determined by measuring cross sectional thickness of intimal (I) and medial (M) tissue of fixed arteries. In untreated animals (n = 5), 14 days after collar positioning an intimal hyperplasia was clearly detectable: the arteries with no collar (sham) showed an I/M tissue ratio of 0.03 +/- 0.02, whereas in the carotid with collar the ratio was 0.62 +/- 0.12. In lacidipine-treated animals a significant and dose-dependent effect on proliferative lesions at all three doses tested, was observed. I/M ratios were 0.47 +/- 0.02, 0.40 +/- 0.09, 0.32 +/- 0.02 for doses 1, 3, and 10 mg kg-1 day-1, respectively (P < 0.05). 4. The fatty lesion extent was significantly reduced by lacidipine at the 10 mg kg-1 day-1 dose, although a trend was also observed with lower dosage. 5. These results suggest a direct antiatherosclerotic effect of lacidipine, independent of modulation of risk factors such as hypercholesterolaemia and/or hypertension. Furthermore, the proliferative lesions are apparently more sensitive to lacidipine than are lipid-rich lesions.

    Topics: Animals; Aorta; Arteriosclerosis; Calcium Channel Blockers; Dihydropyridines; Hypercholesterolemia; Hyperplasia; Lipids; Male; Rabbits

1996
Concomitant aspirin treatment abolishes the antiatherosclerotic effects of the calcium channel blocker isradipine mediated by PGI2.
    Agents and actions. Supplements, 1992, Volume: 37

    108 male rabbits, aged 6 months, with experimental hypercholesterolemia and experimental abdominal aortic lesioning received different regimen of antiatherosclerotic treatment; 36 of them were treated with isradipine, a dihydropyridine calcium antagonist (0.3 mg/kg/daily), 36 with isradipine in combination with aspirin whereas 36 animals received placebo. The entry of 125I-radiolabelled LDL into the aorta was demonstrated to be significantly diminished in isradipine-treated rabbits as well as positive Sudan-III-staining and aortic cholesterol content were in comparison to placebo. This benefit was almost completely abolished by concomitant aspirin-treatment. The notable increase in vascular prostacyclin (PGI2) is supposed to mediate the strong antiatherosclerotic effect of isradipine resulting in an inhibition of LDL-entry and vascular cholesterol accumulation. Aspirin almost totally blocked the raise in PGI2-synthesis by the inhibition of cyclooxygenase detected in isradipine-treated animals. It can be concluded, that aspirin-treatment may minimize the antiatherosclerotic actions of calcium antagonists which are mediated by the PG-system.

    Topics: Animals; Aorta, Abdominal; Arteriosclerosis; Aspirin; Calcium Channel Blockers; Cholesterol; Dihydropyridines; Epoprostenol; Humans; Hypercholesterolemia; Isradipine; Kinetics; Lipid Metabolism; Lipoproteins, LDL; Male; Rabbits

1992