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Jose E Tanussantos - One of the best experts on this subject based on the ideXlab platform.
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Lercanidipine decreases vascular matrix metalloproteinase 2 activity and protects against vascular dysfunction in diabetic rats
European Journal of Pharmacology, 2008Co-Authors: Marcio L L Martinez, Michele M Castro, Elen Rizzi, Karla Fernandes, Lusiane M Bendhack, Raquel F Gerlach, Jose E TanussantosAbstract:Abstract Abnormal matrix metalloproteinases (MMPs) activity causes cardiovascular diseases. Because hyperglycemia increase MMPs activities through increased oxidative stress, we hypothesized that antioxidant effects produced by Lercanidipine could attenuate the increases in MMP-2 expression/activity in diabetic rats. Control and diabetic (alloxan-induced diabetes) rats received Lercanidipine 2.5 mg/kg/day (or tap water) starting three weeks after alloxan (or vehicle) injections. Blood pressure was monitored weekly. After six weeks of treatment, vascular reactivity and structural changes were assessed in aortic rings. MMP-2 levels were determined by gelatin zymography, and MMP-2/tissue inhibitor of metalloproteinases (TIMP)-2 mRNA levels were determined by quantitative real time RT-PCR. Plasma thiobarbituric acid reactive substances concentrations were determined by fluorimetry. Lercanidipine produced antihypertensive effects (201 ± 5 vs. 163 ± 7 mm Hg in diabetic rats untreated and treated with Lercanidipine, respectively; P P P P
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Lercanidipine reduces matrix metalloproteinase 2 activity and reverses vascular dysfunction in renovascular hypertensive rats
European Journal of Pharmacology, 2008Co-Authors: Marcio L L Martinez, Michele M Castro, Elen Rizzi, Karla Fernandes, Caroline Demacq, Lusiane M Bendhack, Raquel F Gerlach, Jose E TanussantosAbstract:Abstract Increased expression/activity of matrix metalloproteinases (MMPs), especially MMP-2, plays a role in the vascular alterations induced by hypertension, and increased oxidative stress is a major factor activating MMPs. Here, we hypothesized that Lercanidipine, a calcium channel blocker, could attenuate the increases in oxidative stress and MMP-2 expression/activity in the two-kidney, one-clip (2K-1C) hypertensive rats. Sham-operated or 2K-1C hypertension rats were treated with Lercanidipine 2.5 mg/kg/day (or vehicle) starting three weeks after hypertension was induced. Systolic blood pressure was monitored weekly. After five weeks of treatment, aortic rings were isolated to assess endothelium-dependent and independent relaxations. Quantitative morphometry of structural changes in the aortic wall were studied in hematoxylin/eosin sections. Aortic MMP-2 levels were determined by gelatin zymography. Aortic MMP-2/tissue inhibitor of metalloproteinases (TIMP)-2 mRNA levels were determined by quantitative real-time RT-PCR. Plasma thiobarbituric acid reactive substances concentrations were determined using a fluorometric method. Lercanidipine attenuated 2K-1C hypertension (224 ± 12 versus 183 ± 11 mm Hg in 2K-1C rats and 2K-1C + Lercandipine rats, respectively; P
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Lercanidipine reduces matrix metalloproteinase 9 activity in patients with hypertension
Journal of Cardiovascular Pharmacology, 2006Co-Authors: Marcio L L Martinez, Raquel F Gerlach, Livia F Lopes, Eduardo Barbosa Coelho, Fernando Nobre, Joao Rocha, Jose E TanussantosAbstract:Abstract:Increased levels of metalloproteinase (MMP)-9 have been shown in hypertensive patients. Lercanidipine is a calcium channel blocker with antioxidant actions. We examined whether Lercanidipine produces antioxidant effects and reduces MMP-9 activity in hypertensive patients in a placebo-contro
Shufen Liou - One of the best experts on this subject based on the ideXlab platform.
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Lercanidipine and labedipinedilol a attenuate lipopolysaccharide interferon γ induced inflammation in rat vascular smooth muscle cells through inhibition of hmgb1 release and mmp 2 9 activities
Atherosclerosis, 2013Co-Authors: Jyh Chong Liang, Ingjun Chen, Shufen LiouAbstract:Abstract Objective Inflammation is an important molecular basis of atherosclerosis. Recent studies have shown that dihydropyridine calcium channel blockers (CCBs) can exert potent anti-inflammatory effects in models of vascular dysfunction. The purpose of the present study was to evaluate anti-inflammatory effects and mechanisms of Lercanidipine and labedipinedilol-A, new generation dihydropyridine CCBs, in rat vascular smooth muscle cells (VSMCs) exposed to lipopolysaccharide (LPS) and interferon-γ (IFN-γ). Methods and results MTT, Griess reagent, RT-PCR, ELISA, gelatin zymography, immunocytochemistry and Western blotting were employed. We found that Lercanidipine and labedipinedilol-A attenuated production of NO, ROS and TNF-α from LPS/IFN-γ-stimulated VSMCs. In addition, they both diminished the LPS/IFN-γ-induced expression of iNOS protein and mRNA, with attenuation of HMGB1 cytosolic translocation and subsequent extracellular release. Furthermore, they down-regulated MMP-2/MMP-9 activities, whereas expression of tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), an inhibitor of MMP-9, was up-regulated. Finally, we found that Lercanidipine and labedipinedilol-A inhibited the nuclear translocation of NF-κB and suppressed the phosphorylation of JNK, p38 MAPK and Akt. Conclusion Lercanidipine and labedipinedilol-A can exert their anti-inflammatory effects through suppression of NO, ROS and TNF-α through down-regulation of iNOS, MMP-2/MMP-9, and HMGB1, with inhibition of signaling transduction of MAPKs, Akt/IkB-α and NF-κB pathways. These findings implicate a valuable role of new generation dihydropyridine CCBs Lercanidipine and labedipinedilol-A for the treatment of inflammatory vascular diseases.
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Lercanidipine inhibits vascular smooth muscle cell proliferation and neointimal formation via reducing intracellular reactive oxygen species and inactivating ras erk1 2 signaling
Pharmacological Research, 2009Co-Authors: Jiunnren Wu, Shufen Liou, Cheeyin Chai, Jyh Chong Liang, Ingjun ChenAbstract:Lercanidipine, a calcium channel antagonist, is currently employed in the treatment of essential hyper- tension and angina pectoris. The purpose of this study was to elucidate the anti-proliferative effect of Lercanidipine and to investigate the molecular role of this agent. Both in vitro studies and in a balloon injury rat carotid artery model were employed to study the effect of Lercanidipine on smooth muscle cell proliferation. Lercanidipine-inhibited rat vascular smooth muscle cell (VSMC) proliferation and migration in a dose-dependent manner following stimulation of VSMC cultures with 10% fetal bovine serum (FBS) and 20 ng/ml platelet-derived growth factor (PDGF)-BB. FBS- and PDGF-BB-stimulated intracellular Ras, MEK1/2, ERK1/2, proliferative cell nuclear antigen (PCNA), and Akt activations were significantly inhibited by Lercanidipine; however, Lercanidipine did not affect FBS- and PDGF-BB-induced STAT3 phosphorylation. Lercanidipine also inhibited PDGF-receptor chain phosphorylation and reactive oxygen species (ROS) production induced by PDGF-BB. Lercanidipine blocked the FBS-inducible progression through the G0/G1 to the S-phase of the cell cycle in synchronized cells. In vivo, 14 days after balloon injury, treatment with 3 and 10 mg/kg Lercanidipine resulted in significant inhibition of the neointima/media ratio. Suppression of neointima formation by Lercanidipine was dependent on its influence on ERK1/2 phosphorylation. These results demonstrate that Lercanidipine can suppress the proliferation of VSMCs via inhibiting cellular ROS, Ras-MEK1/2-ERK1/2, and PI3K-Akt pathways, and suggesting that it may have therapeutic relevance in the prevention of human restenosis.
Ingjun Chen - One of the best experts on this subject based on the ideXlab platform.
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Lercanidipine and labedipinedilol a attenuate lipopolysaccharide interferon γ induced inflammation in rat vascular smooth muscle cells through inhibition of hmgb1 release and mmp 2 9 activities
Atherosclerosis, 2013Co-Authors: Jyh Chong Liang, Ingjun Chen, Shufen LiouAbstract:Abstract Objective Inflammation is an important molecular basis of atherosclerosis. Recent studies have shown that dihydropyridine calcium channel blockers (CCBs) can exert potent anti-inflammatory effects in models of vascular dysfunction. The purpose of the present study was to evaluate anti-inflammatory effects and mechanisms of Lercanidipine and labedipinedilol-A, new generation dihydropyridine CCBs, in rat vascular smooth muscle cells (VSMCs) exposed to lipopolysaccharide (LPS) and interferon-γ (IFN-γ). Methods and results MTT, Griess reagent, RT-PCR, ELISA, gelatin zymography, immunocytochemistry and Western blotting were employed. We found that Lercanidipine and labedipinedilol-A attenuated production of NO, ROS and TNF-α from LPS/IFN-γ-stimulated VSMCs. In addition, they both diminished the LPS/IFN-γ-induced expression of iNOS protein and mRNA, with attenuation of HMGB1 cytosolic translocation and subsequent extracellular release. Furthermore, they down-regulated MMP-2/MMP-9 activities, whereas expression of tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), an inhibitor of MMP-9, was up-regulated. Finally, we found that Lercanidipine and labedipinedilol-A inhibited the nuclear translocation of NF-κB and suppressed the phosphorylation of JNK, p38 MAPK and Akt. Conclusion Lercanidipine and labedipinedilol-A can exert their anti-inflammatory effects through suppression of NO, ROS and TNF-α through down-regulation of iNOS, MMP-2/MMP-9, and HMGB1, with inhibition of signaling transduction of MAPKs, Akt/IkB-α and NF-κB pathways. These findings implicate a valuable role of new generation dihydropyridine CCBs Lercanidipine and labedipinedilol-A for the treatment of inflammatory vascular diseases.
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Lercanidipine inhibits vascular smooth muscle cell proliferation and neointimal formation via reducing intracellular reactive oxygen species and inactivating ras erk1 2 signaling
Pharmacological Research, 2009Co-Authors: Jiunnren Wu, Shufen Liou, Cheeyin Chai, Jyh Chong Liang, Ingjun ChenAbstract:Lercanidipine, a calcium channel antagonist, is currently employed in the treatment of essential hyper- tension and angina pectoris. The purpose of this study was to elucidate the anti-proliferative effect of Lercanidipine and to investigate the molecular role of this agent. Both in vitro studies and in a balloon injury rat carotid artery model were employed to study the effect of Lercanidipine on smooth muscle cell proliferation. Lercanidipine-inhibited rat vascular smooth muscle cell (VSMC) proliferation and migration in a dose-dependent manner following stimulation of VSMC cultures with 10% fetal bovine serum (FBS) and 20 ng/ml platelet-derived growth factor (PDGF)-BB. FBS- and PDGF-BB-stimulated intracellular Ras, MEK1/2, ERK1/2, proliferative cell nuclear antigen (PCNA), and Akt activations were significantly inhibited by Lercanidipine; however, Lercanidipine did not affect FBS- and PDGF-BB-induced STAT3 phosphorylation. Lercanidipine also inhibited PDGF-receptor chain phosphorylation and reactive oxygen species (ROS) production induced by PDGF-BB. Lercanidipine blocked the FBS-inducible progression through the G0/G1 to the S-phase of the cell cycle in synchronized cells. In vivo, 14 days after balloon injury, treatment with 3 and 10 mg/kg Lercanidipine resulted in significant inhibition of the neointima/media ratio. Suppression of neointima formation by Lercanidipine was dependent on its influence on ERK1/2 phosphorylation. These results demonstrate that Lercanidipine can suppress the proliferation of VSMCs via inhibiting cellular ROS, Ras-MEK1/2-ERK1/2, and PI3K-Akt pathways, and suggesting that it may have therapeutic relevance in the prevention of human restenosis.
Pamela Maffioli - One of the best experts on this subject based on the ideXlab platform.
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retracted enalapril Lercanidipine combination on markers of cardiovascular risk a randomized study
Journal of The American Society of Hypertension, 2014Co-Authors: Giuseppe Derosa, Aldo Bonaventura, Davide Romano, Lucio Bianchi, Elena Fogari, Angela Dangelo, Pamela MaffioliAbstract:: The aim of this study was to evaluate enalapril/Lercanidipine combination effects on markers of cardiovascular risk stratification in hypertensive patients. A total of 359 patients were randomized to enalapril 20 mg, Lercanidipine 10 mg, or enalapril/Lercanidipine 20/10 mg fixed combination. We evaluated blood pressure (BP), fasting plasma glucose (FPG), lipid profile, lipoprotein(a) (Lp[a]), soluble receptor for advanced glycation end products (sRAGE), soluble CD40 ligand (sCD40 L), serum myeloperoxidase (MPO), high sensitivity C-reactive protein (Hs-CRP), and tumor necrosis factor-α (TNF-α). We recorded a decrease of BP in all groups, with the enalapril/Lercanidipine combination being more effective in reducing BP compared with single monotherapies. Lipid profile or FPG were not affected by various treatments. Lercanidipine, but not enalapril, improved Lp(a) levels compared with baseline, with enalapril/Lercanidipine having a greater effect on Lp(a) reduction. All treatments increased sRAGE levels, and decreased sCD40 L and MPO, even if enalapril/Lercanidipine combination was more effective than single monotherapies. TNF-α and Hs-CRP were greater reduced by enalapril/Lercanidipine combination compared with enalapril (P < .05 for both). The enalapril/Lercanidipine fixed combination was more effective than single monotherapies in decreasing BP, but also in improving markers of cardiovascular risk stratification in hypertensive patients.
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effects of enalapril Lercanidipine combination on some emerging biomarkers in cardiovascular risk stratification in hypertensive patients
Journal of Clinical Pharmacy and Therapeutics, 2014Co-Authors: Giuseppe Derosa, Aldo Bonaventura, Davide Romano, Lucio Bianchi, Elena Fogari, Angela Dangelo, Pamela MaffioliAbstract:Summary What is known and objective There is considerable interest in pharmacogenetic and molecular biomarkers. Our aim was to evaluate the effects of enalapril/Lercanidipine combination on some emerging biomarkers for cardiovascular risk stratification of hypertensive patients, such as lipoprotein(a) [Lp(a)], soluble advanced glycation end products (sRAGE), soluble CD40 ligand (sCD40L) and serum myeloperoxidase (MPO). Research design and methods Three hundred and forty-five patients were enrolled in this randomized, double-blind, clinical trial: 120 hypertensive patients were randomized to enalapril 20 mg, 110 to Lercanidipine 10 mg and 115 to enalapril/Lercanidipine 20/10 mg fixed combination. We measures the following markers at baseline and after 6, 12, 18 and 24 months: blood pressure, fasting plasma glucose (FPG), lipid profile, Lp(a), sRAGE, sCD40L and MPO. Results There was a decrease in blood pressure in all groups compared with baseline, even if, as expected, enalapril/Lercanidipine combination was more effective in reducing blood pressure compared with the monotherapies. No variations in lipid profile or FPG were recorded in any of the groups. Lercanidipine, but not enalapril, improved Lp(a) levels compared with baseline. The combination enalapril/Lercanidipine improved it more than the single therapies. All treatments increased sRAGE levels, and decreased sCD40L and MPO, with a better effect seen with the enalapril/Lercanidipine combination compared with single monotherapies. What is new and conclusion The combination enalapril/Lercanidipine seems to be better than the single monotherapies in reducing not only blood pressure, but also the levels of some emerging biomarkers, potentially useful for cardiovascular risk stratification of hypertensive patients.
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RETRACTED: Enalapril/Lercanidipine combination on markers of cardiovascular risk: a randomized study
Journal of The American Society of Hypertension, 2014Co-Authors: Giuseppe Derosa, Aldo Bonaventura, Davide Romano, Lucio Bianchi, Elena Fogari, Angela D'angelo, Pamela MaffioliAbstract:: The aim of this study was to evaluate enalapril/Lercanidipine combination effects on markers of cardiovascular risk stratification in hypertensive patients. A total of 359 patients were randomized to enalapril 20 mg, Lercanidipine 10 mg, or enalapril/Lercanidipine 20/10 mg fixed combination. We evaluated blood pressure (BP), fasting plasma glucose (FPG), lipid profile, lipoprotein(a) (Lp[a]), soluble receptor for advanced glycation end products (sRAGE), soluble CD40 ligand (sCD40 L), serum myeloperoxidase (MPO), high sensitivity C-reactive protein (Hs-CRP), and tumor necrosis factor-α (TNF-α). We recorded a decrease of BP in all groups, with the enalapril/Lercanidipine combination being more effective in reducing BP compared with single monotherapies. Lipid profile or FPG were not affected by various treatments. Lercanidipine, but not enalapril, improved Lp(a) levels compared with baseline, with enalapril/Lercanidipine having a greater effect on Lp(a) reduction. All treatments increased sRAGE levels, and decreased sCD40 L and MPO, even if enalapril/Lercanidipine combination was more effective than single monotherapies. TNF-α and Hs-CRP were greater reduced by enalapril/Lercanidipine combination compared with enalapril (P < .05 for both). The enalapril/Lercanidipine fixed combination was more effective than single monotherapies in decreasing BP, but also in improving markers of cardiovascular risk stratification in hypertensive patients.
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Effects of enalapril/Lercanidipine combination on some emerging biomarkers in cardiovascular risk stratification in hypertensive patients.
Journal of Clinical Pharmacy and Therapeutics, 2014Co-Authors: Giuseppe Derosa, Aldo Bonaventura, Davide Romano, Lucio Bianchi, Elena Fogari, Angela D'angelo, Pamela MaffioliAbstract:Summary What is known and objective There is considerable interest in pharmacogenetic and molecular biomarkers. Our aim was to evaluate the effects of enalapril/Lercanidipine combination on some emerging biomarkers for cardiovascular risk stratification of hypertensive patients, such as lipoprotein(a) [Lp(a)], soluble advanced glycation end products (sRAGE), soluble CD40 ligand (sCD40L) and serum myeloperoxidase (MPO). Research design and methods Three hundred and forty-five patients were enrolled in this randomized, double-blind, clinical trial: 120 hypertensive patients were randomized to enalapril 20 mg, 110 to Lercanidipine 10 mg and 115 to enalapril/Lercanidipine 20/10 mg fixed combination. We measures the following markers at baseline and after 6, 12, 18 and 24 months: blood pressure, fasting plasma glucose (FPG), lipid profile, Lp(a), sRAGE, sCD40L and MPO. Results There was a decrease in blood pressure in all groups compared with baseline, even if, as expected, enalapril/Lercanidipine combination was more effective in reducing blood pressure compared with the monotherapies. No variations in lipid profile or FPG were recorded in any of the groups. Lercanidipine, but not enalapril, improved Lp(a) levels compared with baseline. The combination enalapril/Lercanidipine improved it more than the single therapies. All treatments increased sRAGE levels, and decreased sCD40L and MPO, with a better effect seen with the enalapril/Lercanidipine combination compared with single monotherapies. What is new and conclusion The combination enalapril/Lercanidipine seems to be better than the single monotherapies in reducing not only blood pressure, but also the levels of some emerging biomarkers, potentially useful for cardiovascular risk stratification of hypertensive patients.
Giuseppe Derosa - One of the best experts on this subject based on the ideXlab platform.
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retracted enalapril Lercanidipine combination on markers of cardiovascular risk a randomized study
Journal of The American Society of Hypertension, 2014Co-Authors: Giuseppe Derosa, Aldo Bonaventura, Davide Romano, Lucio Bianchi, Elena Fogari, Angela Dangelo, Pamela MaffioliAbstract:: The aim of this study was to evaluate enalapril/Lercanidipine combination effects on markers of cardiovascular risk stratification in hypertensive patients. A total of 359 patients were randomized to enalapril 20 mg, Lercanidipine 10 mg, or enalapril/Lercanidipine 20/10 mg fixed combination. We evaluated blood pressure (BP), fasting plasma glucose (FPG), lipid profile, lipoprotein(a) (Lp[a]), soluble receptor for advanced glycation end products (sRAGE), soluble CD40 ligand (sCD40 L), serum myeloperoxidase (MPO), high sensitivity C-reactive protein (Hs-CRP), and tumor necrosis factor-α (TNF-α). We recorded a decrease of BP in all groups, with the enalapril/Lercanidipine combination being more effective in reducing BP compared with single monotherapies. Lipid profile or FPG were not affected by various treatments. Lercanidipine, but not enalapril, improved Lp(a) levels compared with baseline, with enalapril/Lercanidipine having a greater effect on Lp(a) reduction. All treatments increased sRAGE levels, and decreased sCD40 L and MPO, even if enalapril/Lercanidipine combination was more effective than single monotherapies. TNF-α and Hs-CRP were greater reduced by enalapril/Lercanidipine combination compared with enalapril (P < .05 for both). The enalapril/Lercanidipine fixed combination was more effective than single monotherapies in decreasing BP, but also in improving markers of cardiovascular risk stratification in hypertensive patients.
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effects of enalapril Lercanidipine combination on some emerging biomarkers in cardiovascular risk stratification in hypertensive patients
Journal of Clinical Pharmacy and Therapeutics, 2014Co-Authors: Giuseppe Derosa, Aldo Bonaventura, Davide Romano, Lucio Bianchi, Elena Fogari, Angela Dangelo, Pamela MaffioliAbstract:Summary What is known and objective There is considerable interest in pharmacogenetic and molecular biomarkers. Our aim was to evaluate the effects of enalapril/Lercanidipine combination on some emerging biomarkers for cardiovascular risk stratification of hypertensive patients, such as lipoprotein(a) [Lp(a)], soluble advanced glycation end products (sRAGE), soluble CD40 ligand (sCD40L) and serum myeloperoxidase (MPO). Research design and methods Three hundred and forty-five patients were enrolled in this randomized, double-blind, clinical trial: 120 hypertensive patients were randomized to enalapril 20 mg, 110 to Lercanidipine 10 mg and 115 to enalapril/Lercanidipine 20/10 mg fixed combination. We measures the following markers at baseline and after 6, 12, 18 and 24 months: blood pressure, fasting plasma glucose (FPG), lipid profile, Lp(a), sRAGE, sCD40L and MPO. Results There was a decrease in blood pressure in all groups compared with baseline, even if, as expected, enalapril/Lercanidipine combination was more effective in reducing blood pressure compared with the monotherapies. No variations in lipid profile or FPG were recorded in any of the groups. Lercanidipine, but not enalapril, improved Lp(a) levels compared with baseline. The combination enalapril/Lercanidipine improved it more than the single therapies. All treatments increased sRAGE levels, and decreased sCD40L and MPO, with a better effect seen with the enalapril/Lercanidipine combination compared with single monotherapies. What is new and conclusion The combination enalapril/Lercanidipine seems to be better than the single monotherapies in reducing not only blood pressure, but also the levels of some emerging biomarkers, potentially useful for cardiovascular risk stratification of hypertensive patients.
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RETRACTED: Enalapril/Lercanidipine combination on markers of cardiovascular risk: a randomized study
Journal of The American Society of Hypertension, 2014Co-Authors: Giuseppe Derosa, Aldo Bonaventura, Davide Romano, Lucio Bianchi, Elena Fogari, Angela D'angelo, Pamela MaffioliAbstract:: The aim of this study was to evaluate enalapril/Lercanidipine combination effects on markers of cardiovascular risk stratification in hypertensive patients. A total of 359 patients were randomized to enalapril 20 mg, Lercanidipine 10 mg, or enalapril/Lercanidipine 20/10 mg fixed combination. We evaluated blood pressure (BP), fasting plasma glucose (FPG), lipid profile, lipoprotein(a) (Lp[a]), soluble receptor for advanced glycation end products (sRAGE), soluble CD40 ligand (sCD40 L), serum myeloperoxidase (MPO), high sensitivity C-reactive protein (Hs-CRP), and tumor necrosis factor-α (TNF-α). We recorded a decrease of BP in all groups, with the enalapril/Lercanidipine combination being more effective in reducing BP compared with single monotherapies. Lipid profile or FPG were not affected by various treatments. Lercanidipine, but not enalapril, improved Lp(a) levels compared with baseline, with enalapril/Lercanidipine having a greater effect on Lp(a) reduction. All treatments increased sRAGE levels, and decreased sCD40 L and MPO, even if enalapril/Lercanidipine combination was more effective than single monotherapies. TNF-α and Hs-CRP were greater reduced by enalapril/Lercanidipine combination compared with enalapril (P < .05 for both). The enalapril/Lercanidipine fixed combination was more effective than single monotherapies in decreasing BP, but also in improving markers of cardiovascular risk stratification in hypertensive patients.
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Effects of enalapril/Lercanidipine combination on some emerging biomarkers in cardiovascular risk stratification in hypertensive patients.
Journal of Clinical Pharmacy and Therapeutics, 2014Co-Authors: Giuseppe Derosa, Aldo Bonaventura, Davide Romano, Lucio Bianchi, Elena Fogari, Angela D'angelo, Pamela MaffioliAbstract:Summary What is known and objective There is considerable interest in pharmacogenetic and molecular biomarkers. Our aim was to evaluate the effects of enalapril/Lercanidipine combination on some emerging biomarkers for cardiovascular risk stratification of hypertensive patients, such as lipoprotein(a) [Lp(a)], soluble advanced glycation end products (sRAGE), soluble CD40 ligand (sCD40L) and serum myeloperoxidase (MPO). Research design and methods Three hundred and forty-five patients were enrolled in this randomized, double-blind, clinical trial: 120 hypertensive patients were randomized to enalapril 20 mg, 110 to Lercanidipine 10 mg and 115 to enalapril/Lercanidipine 20/10 mg fixed combination. We measures the following markers at baseline and after 6, 12, 18 and 24 months: blood pressure, fasting plasma glucose (FPG), lipid profile, Lp(a), sRAGE, sCD40L and MPO. Results There was a decrease in blood pressure in all groups compared with baseline, even if, as expected, enalapril/Lercanidipine combination was more effective in reducing blood pressure compared with the monotherapies. No variations in lipid profile or FPG were recorded in any of the groups. Lercanidipine, but not enalapril, improved Lp(a) levels compared with baseline. The combination enalapril/Lercanidipine improved it more than the single therapies. All treatments increased sRAGE levels, and decreased sCD40L and MPO, with a better effect seen with the enalapril/Lercanidipine combination compared with single monotherapies. What is new and conclusion The combination enalapril/Lercanidipine seems to be better than the single monotherapies in reducing not only blood pressure, but also the levels of some emerging biomarkers, potentially useful for cardiovascular risk stratification of hypertensive patients.
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differential effects of Lercanidipine and nifedipine gits on plasma norepinephrine in chronic treatment of hypertension
American Journal of Hypertension, 2003Co-Authors: Roberto Fogari, Giuseppe Derosa, Amedeo Mugellini, Annalisa Zoppi, L Corradi, Andrea Rinaldi, Paola PretiAbstract:Abstract This study aimed to compare the effects of two long-acting dihydropyridine calcium channel blockers (CCBs) with different pharmacologic properties, Lercanidipine and nifedipine Gastro-Intestinal Therapeutic System (GITS), in the chronic treatment of essential hypertension. After a 4-week placebo run-in period, 60 patients of both sexes were randomly treated with Lercanidipine 10 to 20 mg or nifedipine GITS 30 to 60 mg taken orally for 48 weeks, according to a double-blind, parallel group design. For the first 4 weeks of treatment, the lowest dose of each drug was used, followed by higher doses if diastolic blood pressure (BP) was >90 mm Hg. At the end of the placebo period and after 4, 8, 12, 24, and 48 weeks of active treatment BP, heart rate (HR), and plasma norepinephrine (NE) levels were assessed. Lercanidipine and nifedipine GITS similarly reduced BP values after 48 weeks (−21.7/15.9 mm Hg and −20.7/14.6 mm Hg, respectively, both P v placebo), with no change in HR. Despite the similar lack of effect on HR, the two drugs displayed different influences on plasma NE, which was significantly increased by nifedipine GITS (+56 pg/mL, P v placebo) but not by Lercanidipine. These findings suggest that 1) sympathetic activation occurs during chronic therapy with nifedipine GITS but not with Lercanidipine, which might be related to the different pharmacologic characteristics of the two CCBs at the doses evaluated; and 2) nifedipine GITS seems to activate peripheral but not cardiac sympathetic nerves, consistent with differing regulation of cardiac and peripheral sympathetic activity.