Effects Of Felodipine Research Articles

Felodipine in Treatment of Arterial Hypertension and Ischemic Heart Disease

Cardiovascular diseases are the leading cause of death both in the world and in the Russian Federation. The most significant contributors to the increase in mortality are arterial hypertension (AH) and ischemic heart disease (IHD). Dihydropyridine calcium channel blockers (CCBs) are the first line of treatment for these conditions. This is noted in the clinical guidelines for the diagnosis and treatment of AH and in the guidelines for the management of patients with chronic coronary syndromes. CCBs are a heterogeneous group of drugs that have both general and individual pharmacokinetic and pharmacodynamic properties. They are used in patients with AH and/or IHD, including those with concomitant diseases (diabetes mellitus, chronic kidney disease, bronchial asthma, chronic obstructive pulmonary disease, peripheral arterial disease). Felodipine is one of the CCBs. It has a combination of clinical effects, allowing the drug to be prescribed as a first-line therapy for AH, IHD and a combination of these diseases. This is noted in the registered indications for its use. This CCB has a sufficient evidence base of clinical trials demonstrating not only good antihypertensive and antianginal potential of the drug, but also the nephroprotection and cerebroprotection properties. The nephroprotective effect of felodipine is associated with a slowdown in the progression of chronic kidney disease, and the cerebroprotective effect is associated with a decrease in the risk of stroke and an improvement in cognitive functioning. The safety profile of felodipine is favorable: peripheral edema develops much less frequently. This is confirmed by the results of comparative studies. Felodipine is recommended for a wide range of patients with AH, IHD and their combination due to such clinical and pharmacological properties.

Effect of felodipine combined with irbesartan on blood pressure control and carotid artery intima-media thickness in hypertensive patients

Objective To investigate the clinical efficacy of felodipine combined with irbesartan in the treat-ment of hypertension and its effect on atherosclerosis in remission .Methods 100 patients with hypertension were divided into the observation group and the control group .The control group was given the felodipine treatment ,the obser vation group was given felodipine treatment based on the control group .The treatment effect ,changes of blood control and carotid artery intima-media thickness were compared between the two groups .Results The total effective rate of the observation group was 90.0%,which was significantly higher than 72% of the control group （χ2 =3.85,P〈0.05）.After treatment,the systolic pressure,diastolic pressure of the observation group were significantly lower than those in the control group（t=4.21,5.05,all P〈0.05）.After treatment,the size,thickness of carotid artery plaque of the observation group were significantly lower than those of the control group （t =1.98,5.05,all P 〈0.05）. Conclusion Felodipine combined with irbesartan can significantly improve the therapeutic effect of hypertensive patients,and can improve the control of blood pressure ,slow the progression of atherosclerosis . Key words: Hypertension; Atherosclerosis; Felodipine; Irbesartan

Effect of felodipine with irbesartan or metoprolol on sexual function and oxidative stress in women with essential hypertension

To evaluate the impact of felodipine with irbesartan on sexual function compared with felodipine with metoprolol in hypertensive women. This was a prospective, randomized, parallel, active-controlled, open-label study (ClinicalTrials.org: NCT01238705) in 160 women (18-60 years) with mild or moderate hypertension, randomized to a once-daily treatment with felodipine combined with irbesartan or metoprolol for 48 weeks. Patients' sexual function was evaluated using a female sexual function index (FSFI) questionnaire at baseline and after 24 and 48 weeks of therapy. Levels of serum estradiol, testosterone, 8-hydroxy-2'-deoxyguanosine (8-OHdG), 4-hydroxynonenal (4-HNE) and malondialdehyde (MDA) were measured. The two combination regimens were similarly effective in lowering blood pressure. After 48 weeks, in felodipine-irbesartan group, total scores of FSFI improved (P < 0.001). Items showing improvement in scores corresponded to desire, arousal and orgasm (P < 0.001; P = 0.002; P = 0.049, respectively). Levels of estradiol increased under treatment with felodipine-irbesartan (P = 0.003) and decreased under felodipine-metoprolol treatment (P < 0.001). The concentration of testosterone declined after felodipine-irbesartan therapy (P < 0.001) and increased under felodipine-metoprolol treatment (P < 0.001). In the felodipine-irbesartan group, decreases of 8-OHdG, 4-HNE (P < 0.001) and MDA (P < 0.001) were observed. The felodipine-irbesartan combination resulted in less oxidative stress. The differences in changes in 8-OHdG, 4-HNE and MDA between the two groups were significant (P < 0.05). These results suggested that the felodipine-irbesartan combination regimen improved sexual function in hypertensive women, whereas felodipine-metoprolol regiment did not. The reason for the different influence of these two combination therapy on female sexual function might be their different impacts on oxidative stress and hormone levels.

Felodipine downregulates serum interleukin-18 levels in rats with fructose-induced metabolic syndrome

Human studies suggest that calcium-channel blockers have cardiovascular protection besides reducing blood pressure, and interleukin-18 (IL-18) levels which are elevated in obese population are associated with metabolic syndrome (MetS). The purpose of this research was to study the change of serum IL-18 levels and the effect of felodipine on it in high-fructose diet-fed rats. In this research, 30 Wistar male rats were randomized into 3 groups. A control group (no.=12) was fed with normal feeds, and high-fructose diet was given to a fructose group and a flodioine group (no.=9 in each group). All animals were fed for a period of 32 weeks, during which body weight and systolic blood pressure (BP) were measured once every 4 weeks. Felodipine (5 mg/kg/d) was then administered by gavage daily for 6 weeks to the felodipine group. Before and after treatment with felodipine, fasting plasma lipid, blood glucose, plasma insulin, and serum IL-18 were detected. Body weight, systolic BP, triglycerides, fasting insulin, and the R-value of homeostasis model (HOMA-R) were significantly increased in high-fructose rats (p<0.01). Serum IL-18 levels were elevated and had significant positive correlation with HOMA-R in rats with fructose-induced MetS (p<0.01). We also found that felodipine may decrease HOMA-R and serum IL-18 levels besides reducing blood pressure (p<0.05, p<0.01). IL-18 plays an important role in the development of MetS, while felodipine exerts an anti-inflammatory effect on rats with fructose-induced MetS by downregulating serum IL-18 levels.

Effect of felodipine on the serum lipid profile of patients with hypertension

Forty patients suffering from mild to moderate degree of hypertension were put on felodipine. Their lipid profile was analysed before the start of their therapy and consecutively at two and four months after starting felodipine. There was a statistically significant fall in the levels of serum cholesterol, serum triglycerides and serum total lipids; though no appreciable variation was observed in HDL and LDL cholesterol levels. At baseline there were a few patients who had higher than the normal range of the serum lipid profile. Analysis of these patients showed a highly significant fall in the levels of serum cholesterol, serum triglycerides, serum LDL-cholesterol and serum total lipids i.e. felodipine modified the lipid profiles of hypertensive patients in a positive way.

Felodipine in Patients with Organic Solvent-Induced Chronic Toxic Encephalopathy

Objective: The aim of this investigation was to study the effect of felodipine extended release (ER) 5 and 10mg once daily compared with placebo on performance in psychometric testing and Target Complaints in patients with toxic encephalopathy (TE). Design: The study was conducted as a double-blind, crossover study with each treatment given for 6 weeks. The patients were examined on five occasions, using semistructured interviews (Target Complaints), questionnaires [Psychological General Well-Being Index (PGWB)] and psychometric tests of visuo-spatial capacity and memory functioning. Patients: Twelve male patients with organic solvent-induced chronic TE and a median age of 47 years. All were skilled workers who had been exposed to organic solvents for a median of 26 years (range 9 to 39 years). The baseline examinations revealed severe symptoms such as memory impairment, sleep disturbance and personality change. Impaired test performance and reduced cerebral blood flow were also noted. Because of the severity of the symptoms only 3 patients were able to work (part-time). Results: No difference was observed between felodipine treatment and placebo in the psychometric testing and the PGWB index. However, in the Target Complaints a statistically significant (p < 0.05) reduction of the severity of the symptoms was noted when the patients were treated once daily with felodipine ER 5mg compared with placebo. This reduction was especially pronounced in five of the patients, the so-called responders. Conclusion: The findings indicate that felodipine can be used in the treatment of TE patients to reduce their symptoms.

Renal hypoxanthine balance in cardiac surgery: Effects of felodipine

Objective: To test the hypothesis that felodipine, a renal vasodilator, can prevent a release of hypoxanthine during rewarming after moderate hypothermic cardiopulmonary bypass and that this is related to improved renal oxygen supply. Design: A prospective, randomized, and controlled study. Setting: Operating room in the cardiothoracic surgery department of a university hospital. Participants: Twenty-two patients submitted to elective first-time coronary bypass surgery. Interventions: A catheter was placed in the left renal vein for thermodilution renal blood flow (RBF) measurement and blood sampling. In 11 patients, felodipine was infused during the hypothermic period of cardiopulmonary bypass. Measurements and Main Results: Renal uptake (renal arteriovenous concentration difference × RBF) of hypoxanthine was maintained during rewarming in felodipine-treated patients but not in control patients (55 ± 28 v −39 ± 1 nmol/ min, p < 0.05). Oxygen consumption was higher after felodipine infusion despite unchanged total RBF. A positive correlation between renal oxygen consumption and hypoxanthine uptake and release ( r = 0.74, p < 0.01) was observed. Conclusions: Felodipine maintained renal uptake of hypoxanthine during rewarming after hypothermic cardiopulmonary bypass. This maintenance is the effect of improved renal oxygen supply secondary to improved nutritive blood flow at the expense of nonnutritive renal blood flow.

Divergent effects of felodipine on nitric oxide synthase (NOS) expression in different forms of hypertension in rats.

Divergent effects of felodipine on nitric oxide synthase (NOS) expression in different forms of hypertension in rats.

Effect of Felodipine on Arterial Blood Flow and Venous Function at Rest in Patients with Mild Essential Hypertension

Felodipine is a second-generation dihydropyridine calcium antagonist used to treat mild to moderate arterial hypertension. The authors used venous occlusion plethysmography to study the effect of this drug on lower limb arterial inflow and venous outflow in 10 at rest patients with mild essential hypertension. They also sought correlations between changes in district blood flow and blood pressure. Plethysmography was carried out at 8 AM and 4, 8, and 24 hours later at baseline (after washout), on the first day of treatment with a single daily administration of 10 mg felodipine ER, and after 7 and 30 days of treatment. The drug was given after the 8 AM evaluation. The authors determined rest flow, maximal venous incremental volume (MVIV) at 40 mmHg and 60 mmHg, and gradient of venous volume between 60 and 40 mmHg divided by the pressure difference (DV/DP) as index of venous distensibility. On the days of plethysmographic evaluation, arterial blood pressure and heart rate were measured continuously over 24 hours by the ABPM (Ambulatory Blood Pressure Monitoring). The results were analyzed by ANOVA. Rest flow, MVIV, and DV/DP were stable at the baseline evaluation. On days 1, 7, and 30 of treatment the rest flow after 4 and 8 hours was significantly greater than at 8 AM but had always returned to normal after 24 hours. No other plethysmographic parameters changed significantly; in particular venous outflow remained unchanged. Mean arterial, systolic, and diastolic blood pressure were significantly reduced, compared with baseline, following treatment on the first day and after 7 and 30 days' treatment. There was no effect on heart rate. The authors conclude that felodipine is useful for the treatment of mild essential hypertension, since it reduces arterial resistance without altering venous capacitance or distensibility.

Effects of Felodipine and Enalapril on Coronary Hemodynamics and Myocardial Collagen Content in Aged Spontaneously Hypertensive Rats

Effects of Felodipine and Enalapril on Coronary Hemodynamics and Myocardial Collagen Content in Aged Spontaneously Hypertensive Rats

Effects of felodipine and enalapril on coronary hermodynamics and myocardial collagen content in aged spontaneously hypertensive rats

Effects of felodipine and enalapril on coronary hermodynamics and myocardial collagen content in aged spontaneously hypertensive rats

The effect of felodipine on endothelin-1 levels, peripheral vasoconstriction and flap survival during microvascular breast reconstruction

Endothelin-1 (ET-1) may contribute to vasoconstriction and flap blood flow during microvascular surgery. Calcium antagonists have suppressed ET-1 release in some studies. The effect of 5 mg of felodipine, a vasodilating calcium antagonist, administered the evening and morning before a microvascular TRAM (transverse rectus abdominis musculocutaneous) flap breast reconstruction, on perioperative plasma ET-1 concentrations, peripheral temperature gradient (Tgrad), rectal temperature (T rect), flap skin blood flow with transcutaneous oxygen tension (p tcO 2), heart rate (HR) and mean arterial pressure (MAP) was evaluated in this clinical, randomised, double blind, prospective study. Felodipine did not cause any statistically significant changes in ET-1 levels, Tgrad, T rect, P tcO 2, flap survival or pre- or intraoperative MAP HR was significantly higher in the felodipine group before induction and at 10 min postoperatively. We conclude that in patients undergoing a microvascular TRAM flap breast reconstruction, preoperatively administered felodipine has no effect on perioperative ET-1 levels, temperature changes, or flap skin blood flow.

D101 Effect of felodipine on progression of ventricular dysfunction and symptoms in patients with ischemic mild heart failure chronically treated with enalapril

D101 Effect of felodipine on progression of ventricular dysfunction and symptoms in patients with ischemic mild heart failure chronically treated with enalapril

Beneficial effects of felodipine on myocardial and coronary function during low-flow ischemia and reperfusion

An acute coronary occlusion causes severe low-flow ischemia in the occluded region. Calcium antagonists have the potential to reduce the rate of ischemic injury by decreasing myocardial oxygen demand, as well as by other mechanisms, especially when given prior to the onset of ischemia. However, their clinical use may be limited by their negative inotropic effects. The purpose of this study was to assess the effects of felodipine as a potentially protective agent against myocardial ischemia and reperfusion injury, independent of any negative inotropic actions, when given after the onset of low-flow ischemia. Isolated isovolumic (balloon-in-LV), blood-perfused rabbit hearts, paced at a constant heart rate, were subjected to 90 minutes of low-flow ischemia at a coronary perfusion pressure of 10 mmHg, which reduced coronary blood flow to 22-24% of baseline. After 15 minutes of low-flow ischemia, hearts received 2 x 10(-6) M felodipine (n = 7) or no drug (controls, n = 8). Felodipine was given until 15 minutes of reperfusion. During low-flow ischemia both groups of hearts had identical coronary blood flow, heart rate, left ventricular (LV) developed pressure, lactate production, and O2 consumption. However, felodipine markedly protected against ischemic diastolic dysfunction. At the end of low-flow ischemia, LV end-diastolic pressure (LVEDP) had increased from 10 +/- 1 to 28 +/- 5 mmHg in the felodipine group, while in the controls LVEDP increased to 48 +/- 8 mmHg (p < 0.05). During 30 minutes of reperfusion, felodipine had a beneficial effect upon coronary blood flow (initial postischemic hyperemia 245 +/- 38% of baseline in the felodipine group vs. 124 +/- 18% in the controls; p < 0.01) Felodipine markedly improved the recovery of contractile function [LV developed pressure recovered from a baseline of 104 +/- 4 to 75 +/- 6 mmHg (72%) in the felodipine group vs. 34 +/- 10 mmHg (32%) in the control group; p < 0.01], as well as diastolic function (LVEDP = 25 +/- 4 mmHg in the felodipine group vs. 61 +/- 10 mmHg in the controls; p < 0.05), and ATP levels (8.5 +/- 1.4 mumoles/g d.w. in the felodipine group vs. 3.9 +/- 1.4 mumoles/g d.w. in the control group, p < 0.05). Felodipine, given after the onset of low-flow ischemia, protects the myocardium during both ischemia and reperfusion by mechanisms other than reducing myocardial oxygen demand.

Effects of felodipine on the ischemic heart: insight into the mechanism of cytoprotection.

To assess whether the administration of felodipine protects the myocardium in a dose-dependent manner against ischemia and reperfusion, isolated rabbit hearts were infused with three different concentrations of felodipine: 10(-10), 10(-9), and 10(-8) M. Diastolic and developed pressures were monitored; coronary effluent was collected and assayed for CPK activity and for noradrenaline concentration; mitochondria were harvested and assayed for respiratory activity; and ATP production and calcium content and tissue concentration of ATP, creatine phosphate (CP), and calcium were determined. The occurrence of oxidative stress during ischemia and reperfusion was also monitored in terms of tissue content and release of reduced (GSH) and oxidized (GSSG) glutathione. Treatment with felodipine at 10(-10) and 10(-9) M had no effect on the hearts when perfused under aerobic conditions, whilst the higher dose reduced developed pressure from 57.7 +/- 2.6 to 30.0 +/- 2.6 mmHg (p < 0.01). On reperfusion treated hearts recovered better than the untreated hearts with respect to left ventricular performance, replenishment of ATP and CP stores, and mitochondrial function. Recovery of developed pressure was 100% at 10(-8) M, 55% at 10(-9) M, and 46% at 10(-10) M. The reperfusion-induced tissue and mitochondrial calcium overload, release of CPK and noradrenaline, and oxidative stress were also significantly reduced. The effects of felodipine were dose dependent. Felodipine inhibited the initial rate of ATP-driven calcium uptake but failed to affect the initial rate of mitochondrial calcium transport. It is concluded that felodipine infusion provides dose-dependent protection of the heart against ischemia and reperfusion. Because this protection also occurred at 10(-9) M and 10(-10) M in the absence of a negative inotropic effect during normoxia and of a coronary dilatory effect during ischaemia, it cannot be attributed to an energy-sparing effect or to improvement in oxygen delivery. From our data we can envisage two other major mechanisms-(1) membrane protection and (2) reduction in oxygen toxicity. The ATP-sparing effect occurring at 10(-8) M is likely to be responsible for the further protection.

Felodipine inhibits intimal lesion formation in the hypercholesterolemic rabbit: differential effects on endothelial and monocyte determinants of atherogenesis.

The purpose of this study was to determine if the calcium entry antagonist felodipine inhibited intimal lesion formation in hypercholesterolemic rabbits, and to determine if this was due to an effect upon monocyte and/or endothelial determinants of this interaction. Twenty-three male New Zealand White rabbits received the following treatment regimen for 10 weeks: normal chow (NP, n = 3); normal chow with felodipine infusion (NF, n = 6); 0.5% cholesterol chow (CP, n = 7); or 0.5% cholesterol chow and felodipine infusion (CF, n = 7). After 10 weeks blood was collected for biochemical measurements and mononuclear cell binding assays, and thoracic aortae were harvested for vascular reactivity studies and histomorphometry. In the animals receiving normal chow, felodipine did not significantly affect blood pressure, plasma cholesterol levels, binding studies, vascular reactivity, or structure; therefore these animals were analyzed as one group (N). Plasma cholesterol levels were significantly elevated in groups receiving the 0.5% cholesterol diet (N, 29 +/- 3 mg/dl; CP, 1221 +/- 73 mg/dl; CF, 979 +/- 108 mg/dl). High-density lipoprotein cholesterol was not different between the groups (25 +/- 4 vs 23 +/- 4 vs 27 +/- 4 mg/dl; N vs CF vs CP respectively; p = NS). Cholesterol feeding markedly augmented the adhesiveness of mononuclear cells, as demonstrated by a 250% increase in cell binding. Felodipine did not alter the adhesiveness of mononuclear cells in hypercholesterolemic animals. Cholesterol feeding significantly impaired endothelium-dependent relaxations. Endothelium-dependent relaxations were restored by felodipine treatment as reflected by the maximal responses to acetylcholine (40 +/- 7% vs 58 +/- 4% vs 67 +/- 5%; CP vs CF vs N respectively). The improvement in endothelium-dependent relaxation in the felodipine-treated animals was associated with a 2.2-fold reduction in lesion surface area of the thoracic aorta (8.2 +/- 6.3% vs 18.2 +/- 9.5%; CF vs CP; p < 0.01). Moreover, the intima/media ratio reflecting lesion thickness was substantially reduced by felodipine treatment (0.05 +/- 0.02 vs 0.20 +/- 0.07; CF vs CP; p = 0.006). Ex vivo studies revealed that felodipine inhibited the adhesiveness of vascular endothelium, but not mononuclear cells, derived from hypercholesterolemic animals. Low-dose felodipine appears to inhibit monocyte-endothelial interaction, as indicated by a reduction in the formation of lesions in hypercholesterolemic animals. This effect is not due to an alteration in adhesiveness of mononuclear cells. The salutary effect of felodipine is associated with an increase in vascular nitric oxide activity which may reduce endothelial adhesiveness.

Renal Function During Cardiopulmonary Bypass

Glomerular filtration and tubular activity are decreased during hypothermic cardiopulmonary bypass (CPB). The role of vasoconstriction to explain these changes is not known. The calcium entry blocking drug felodipine dilates constricted arterioles and reduces renal vascular resistance during noncardiac surgery. The present study was initiated to evaluate the effects of felodipine on renal perfusion and function during hypothermic, low pressure CPB. Twenty-two male patients (aged 61.7 +/- 2.3 y) were included in a prospective, randomized, controlled study. Renal blood flow was measured with thermodilution technique; renal extraction of 51Cr-EDTA and p-aminohippurate (PAH) were used to evaluate glomerular and tubular function. Systemic blood flow during hypothermic CPB was varied experimentally between 1.45 and 2.2 L.min-1.m-2. Felodipine reduced systemic vascular resistance but did not reduce the total renal vascular resistance during CPB. On the contrary, renal vascular resistance was increased at low CPB flow rates. The extraction of PAH (signifying tubular activity) was higher during felodipine infusion (0.74 +/- 0.04 vs 0.64 +/- 0.03 during low CPB flow, and 0.64 +/- 0.03 vs 0.57 +/- 0.05 during high CPB flow), whereas 51Cr-EDTA extraction was not influenced. The mechanism of enhanced PAH extraction may involve reduced regional vasoconstriction in PAH-extracting areas.

Noninvasive tracking of coronary atherosclerosis by electron beam computed tomography: Rationale and design of the Felodipine Atherosclerosis Prevention Study (FAPS)

The Felodipine Atherosclerosis Prevention Study is designed to evaluate the efficacy of the calcium antagonist felodipine ER and combined felodipine/simvastatin therapy on retarding the progression or atherosclerosis, estimated by serial changes in coronary calcium evaluated by noninvasive electron beam computed tomography. Subjects include 180 men and women aged 40 to 69 and 50 to 69 years, respectively, with moderate type lla dyslipidemia, with either cardiovascular disease or risk factors. All subjects receive simvastatin lipid-lowering therapy, and are randomized either to felodipine or placebo for a treatment period of 2 years. Monitoring of blood chemistry, measures of lipids and apolipoproteins, blood pressure, evaluation of symptoms, and interim clinical event monitoring are done at routine follow-up visits. Baseline and 2-year follow-up electron beam computed tomography, measuring changes in total calcium score, area, and mass, evaluate the effects of intervention on the progression of calcified atherosclerosis. The results from the Felodipine Atherosclerosis Prevention Study will provide valuable information about the effect of felodipine alone and in combination with simvastatin on progression of calcified atherosclerosis evaluated noninvasively.

Protection against hypoxic injury of rat proximal tubules by felodipine via a calcium-independent mechanism

Most evidence for a key role of calcium entry in hypoxia-induced renal damage stems from studies with calcium channel blockers. In proximal tubules, a primary site of renal ischaemic injury, only phenyl-alkylamines, especially verapamil, have been studied. In the present study the effect of the dihydropyridine felodipine on hypoxic injury in isolated rat proximal tubules was investigated. To discriminate between the block of calcium entry and other effects, the enantiomers and a non-calcium blocking derivative of felodipine (H186/86) were included. Cell membrane injury was assessed by measuring the release of lactate dehydrogenase (LDH). At high concentrations (100 microM) felodipine, H186/86 and the two enantiomers all protected rat proximal tubules against hypoxia-induced injury to the same extent. Absence of extracellular calcium did not offer protection, but rather enhanced hypoxic injury. All dihydropyridines used increased the intracellular potassium concentration during normoxia. Felodipine attenuated the hypoxia-induced loss of cellular potassium. We have tried to mimic the effects of felodipine by using potassium channel blockers. The potassium channel blockers quinidine and glibenclamide afforded some protection against hypoxic injury, although their effects on cellular potassium were equivocal. We conclude that the dihydropyridine calcium channel blocker felodipine protects rat proximal tubules against hypoxic injury via a calcium-independent mechanism. We propose that high levels of intracellular potassium and attenuation of potassium loss during hypoxia are important in this protection.

The effects of felodipine and amlodipine on glucose and lipid metabolism in patients affected by non—insulin-dependent diabetes mellitus and hypertension: a comparative, randomized, parallel-group study

Fifty-three patients with non—insulin-dependent diabetes mellitus and hypertension were randomly treated with extended-release felodipine 10 mg/d, amlodipine 10 mg/d, or placebo for 6 weeks. Mean clinostatic systolic and diastolic blood pressures were significantly reduced from baseline with both drug treatments ( P < 0.0001), whereas placebo affected only systolic pressure. Neither felodipine nor amlodipine treatment led to any significant change in glucose tolerance (as measured by using the oral glucose tolerance test), C-peptide secretion, fructosamine, or glycated hemoglobin A 1c levels. Similarly, neither treatment appeared to increase triglyceride levels, total cholesterol levels, or its fractions. All safety parameters remained stable during the study. There was no significant trend in electrocardiogram (ECG) variations for any of the treatments, but one patient in the amlodipine group showed ECG signs compatible with acute myocardial infarction. These data suggest that in diabetic hypertensive patients, both felodipine and amlodipine have a neutral effect on glucose and lipid metabolism while retaining their hemodynamic efficacy. Therefore, their use as first-step antihypertensive therapies can be recommended in such patients.