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PubMed2006

Liquid chromatography-tandem mass spectrometry validated method for the estimation of indapamide in human whole blood.

A highly precise and sensitive method for the estimation of indapamide in human whole blood using high-performance liquid chromatography-tandem mass spectrometry (LC-MS/MS) is described. The method developed is validated in human whole-blood matrix, with a sensitivity of 0.5 ng/ml as lower limit of quantification. The procedure for the extraction of indapamide and glimepiride as internal standard (IS) involves haemolysis and deprotienation of whole blood using ZnSO(4) followed by liquid-liquid extraction using ethyl acetate. The sample extracts after drying were reconstituted and analysed by LC-MS/MS, equipped with turbo ion spray (TIS) source, operating in the positive ion and selective reaction monitoring (SRM) acquisition mode to quantify indapamide in human whole blood. The mean recovery for indapamide was 82.40 and 93.23% for IS. The total run time was 2.5 min to monitor both indapamide and the IS. The response of the LC-MS/MS method for indapamide was linear over the range of 0.5-80.0 ng/ml with correlation coefficient, r>or=0.9991. The coefficient of variance (% CV) at 0.5 ng/ml was 4.02% and the accuracy was well within the accepted limit of +/-20% at 0.5 ng/ml and +/-15% at all other concentrations in the linear range. This method is fully validated for the accuracy, precision and stability studies and also applied to subject-sample analysis of bioequivalence study for 1.5mg sustained-release (SR) formulations.

Antihypertensive Agents↗
PubMed2005

A selective HPLC method for the determination of indapamide in human whole blood: application to a bioequivalence study in Chinese volunteers.

Indapamide was extracted from human whole blood with diethyl ether and was determined by a HPLC-UV method using an Inertsil ODS-3 column and an isocratic mobile phase consisting of 55% buffer solution (2 g KH(2)PO(4), 3 ml H(3)PO(4) and 3.5 ml triethylamine in 1l of H(2)O), 40% acetonitrile and 5% methanol for 12.5 min, and then a gradient flush from 100% isocratic to a mixture of 20% isocratic mobile phase and 80% methanol for 3 min. Indapamide and glipizide (internal standard) were eluted from the column at about 10.5 and 12.8 min, respectively. The method had within day precision values in the range +/- 1.2 to +/- 9.7% (n = 5) and between day precision in the range +/- 3.3 to +/- 9.7%. The method was linear over the range of 10-400 ng/ml of indapamide in blood (R = 0.999). The LOQ (s/n = 10) of the method was 10 ng/ml. The method was applied in a study of the pharmacokinetics and bioequivalence of generic indapamide capsules (2.5 mg) in comparison with reference indapamide tablets (2.5mg), in 20 healthy male Chinese volunteers. The mean values of major pharmacokinetic parameters of C(max), AUC(0-48), AUC(0-infinity), T(max), and t(1/2) of indapamide in healthy male Chinese volunteers after po a single 5 mg dose for the test product were 331.0 +/- 39.2 ng/ml, 6,193.7+/-873.5 ng h/ml, 7311.8+/-1,232.3 ng h/ml, 3.2+/-0.9h, and 17.3+/-2.8 h, respectively. There was no significant differences between the two formulations.

Area Under Curve↗
PubMed2006

A sensitive LC-ESI-MS method for the determination of indapamide in human plasma: method and clinical applications.

A sensitive LC-ESI-MS method for the determination of indapamide in human plasma using glibenclamide as the internal standard (IS) was established. Following acidification with 1 M hydrochloric acid solution, plasma samples were extracted with ethyl acetate and separated on a C(18) column with a mobile phase of 10 mM ammonium acetate-methanol (22:78, v/v). Indapamide was determined using electrospray ionization in a single quadrupole mass spectrometer. LC-ESI-MS was performed in the selected ion monitoring (SIM) mode using target ions at m/z 364.3 for indapamide and m/z 492.4 for the IS. Calibration curves were linear over the ranges of 0.1-100 ng/ml for indapamide. The lower limit of quantification was 0.1 ng/ml. The intra- and inter-assay precisions were less than 9.5% and 10.6%, respectively. The mean plasma extraction recovery of indapamide was 90.5-93.9%. The method has been successfully applied to study the pharmacokinetics of indapamide in healthy male Chinese volunteers.

Administration, Oral↗
PubMed1998

Fixed low-dose perindopril-indapamide combination in hypertensive patients with chronic renal failure.

The angiotensin converting enzyme inhibitor perindopril and the diuretic indapamide have been shown to be effective antihypertensive agents in patients with chronic renal failure. A fixed low-dose combination of these two agents has been proposed in the treatment of hypertension. We evaluated this combination in 26 patients with mild to moderate essential hypertension and mild to severe chronic renal failure that did not require dialysis. This was a multicenter, open trial consisting of a 2-week single-blind placebo washout period followed by 12 weeks of active treatment. At week 0, the patients received 2 mg perindopril/0.625 mg indapamide once a day or every other day, with the possibility of dosage adjustment to perindopril 4 mg/indapamide 1.25 mg at week 2, week 4, or week 8. A pharmacokinetic analysis using a population pharmacokinetic approach was performed at week 8. Twenty-three patients completed the 12-week study, at which time 14 patients were receiving 2 mg perindopril/0.625 mg indapamide daily, three were receiving 2 mg perindopril/0.625 mg indapamide every other day, and six perindopril 4 mg/indapamide 1.25 mg. Blood pressure readings (supine) decreased from 170.4+/-19.2 / 101.5+/-6.7 mm Hg before active treatment to 146.5+/-19.7 / 86.5+/-10.6 mm Hg at the end of treatment (P < .0001). Pharmacokinetic analysis showed that for indapamide and perindoprilat (the active metabolite of perindopril) the area under the curve (AUC24) increased with the severity of renal failure. No interaction was noted between the two drugs. Mean serum creatinine and sodium and serum potassium levels remained stable during the study. Impairment of renal function occurred in one patient and was considered unrelated to treatment. We conclude that a fixed low-dose perindopril-indapamide combination as first-line treatment has a good safety/efficacy ratio in hypertensive patients with chronic renal failure.

Adolescent↗
PubMed2001

A comparison of indapamide SR 1.5 mg with both amlodipine 5 mg and hydrochlorothiazide 25 mg in elderly hypertensive patients: a randomized double-blind controlled study.

OBJECTIVE: To analyse the efficacy of indapamide sustained-release (SR) 1.5 mg in reducing blood pressure versus amlodipine 5 mg and hydrochlorothiazide 25 mg, in elderly hypertensive patients. DESIGN: Double-blind, randomized, 12 week study using three parallel groups. SETTING: European teaching hospitals and general practices. PATIENTS: Randomized patients, (n = 524) including 128 patients with isolated systolic hypertension (ISH); mean age: 72.4 years; mean systolic/diastolic blood pressures (SBP/DBP): 174.5/97.9 mmHg. MAIN OUTCOME MEASURES: Clinic systolic and diastolic blood pressure variations. RESULTS: Indapamide SR 1.5 mg demonstrates a similar efficacy to that of amlodipine 5 mg, as well as to that of hydrochlorothiazide 25 mg (equivalence P < 0.001); the mean decreases in SBP/DBP were -22.7/-11.8 mmHg, -22.2/-10.7 mmHg and -19.4/-10.8 mmHg, respectively. In the ISH subgroup, indapamide SR 1.5 mg tends to have greater efficacy than hydrochlorothiazide 25 mg in reducing the SBP (-24.7 versus -18.5 mmHg, respectively; equivalence P = 0.117), while similar results are obtained with amlodipine 5 mg (-23 mmHg, equivalence P < 0.001). The normalization rate was relatively high for indapamide SR 1.5 mg (75.3%), when compared with amlodipine (66.9%) and hydrochlorothiazide (67.3%), especially in the subgroup of isolated systolic hypertensive patients: 84.2 versus 80.0% for amlodipine, and versus 71.4% for hydrochlorothiazide. CONCLUSIONS: Indapamide SR 1.5 mg shows similar antihypertensive efficacy to amlodipine 5 mg and hydrochlorothiazide 25 mg in elderly hypertensive patients, while in patients with isolated systolic hypertension, indapamide SR 1.5 mg shows a similar efficacy to amlodipine 5 mg but a greater efficacy than hydrochlorothiazide 25 mg.

Aged↗
PubMed1992

In vitro and ex vivo inhibition of the modification of low-density lipoprotein by indapamide.

The effect of an antihypertensive drug, indapamide, on copper- and endothelial cell-induced peroxidation of human low-density lipoprotein (LDL) was studied and compared with that of drugs previously shown to protect LDL against peroxidation: probucol and vitamin E and other thiazidic and nonthiazidic diuretics (clopamide, hydrochlorothiazide, and furosemide). Incubation with indapamide inhibited in a dose-dependent manner LDL peroxidation induced either by copper ions or by cultured endothelial cells. Both electrophoretic mobility and thiobarbituric acid-reactive substances (TBARS) content of LDL returned to almost normal values in the presence of 1 microM indapamide. This drug was at least 10 times more potent than probucol and vitamin E in inhibiting LDL peroxidation. No inhibitory effect has been observed with clopamide, hydrochlorothiazide, and furosemide in the same experimental conditions. Homozygote Watanabe rabbits were treated orally with indapamide (10 mg/kg/d for 3 days) to evaluate the potential protective effect of the compound on LDL peroxidation in vivo. Purified LDL from placebo and treated rabbits were submitted to peroxidation induced by copper ions, and indapamide was effectively able to protect LDL in these experimental conditions. This effect was especially obvious 6 and 8 h after the start of the incubation when LDL of the placebo-treated animals were modified. The mechanism of action of these drugs was examined in vitro using the 1,1-diphenyl-2-picryl-hydrazyl (DPPH) test and in kinetic studies of arachidonic acid photoperoxidation. Indapamide as well as vitamin E and probucol were effective free radical scavengers, but the other diuretic molecules were not.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Influence of indapamide and chlorthalidone on reperfusion-induced ventricular fibrillation in isolated guinea pig hearts.

The delayed rectifier potassium current (IK) is a major repolarizing current in guinea pig ventricular myocytes. Blockade of IK or other repolarizing currents is of increasing interest for development of antiarrhythmic drugs; however, these interventions may also be proarrhythmic. In the present study, we compared the potential antiarrhythmic properties of indapamide and chlorthalidone, two structurally related sulfonamide diuretics which differ in their ability to block the slow component of the delayed rectifier (IKs) in isolated, buffer-perfused guinea pig hearts. Hearts underwent 30-min global no-flow ischemia and 10-min reperfusion. Dose-response (10(-7)-10(-4) M) effects of indapamide or chlorthalidone on reperfusion-induced arrhythmias, coronary flow, and heart rate (HR) were evaluated in a randomized blinded fashion. There was no significant difference in the incidence of ventricular fibrillation (VF) for either compound as compared with untreated controls. However, VF duration was reduced to < 40 s in all hearts treated with indapamide 10(-4) M). Mean VF duration with indapamide 10(-4) M was 31 +/- 4 versus 70 +/- 40 s in controls (p < 0.05). Chlorthalidone did not protect against reperfusion-induced arrhythmias. HR was unchanged with either compound; coronary flow during the control perfusion period increased approximately 43% with indapamide 10(-4) M (p < 0.05 vs. all treatment groups). These results demonstrate that indapamide, but not chlorthalidone, confers significant protection against reperfusion-induced VF in this experimental preparation and suggest that selective block of IKs may be antiarrhythmic.

Analysis of Variance↗
PubMed2004

Equivalence of indapamide SR and enalapril on microalbuminuria reduction in hypertensive patients with type 2 diabetes: the NESTOR Study.

OBJECTIVES: To test whether microalbuminuria in patients with type 2 diabetes and hypertension is primarily dependent on the severity of hypertension, and to compare the effectiveness of two antihypertensive drugs with opposite effects on the renin-angiotensin system [the diuretic, indapamide sustained release (SR), and an angiotensin-converting enzyme inhibitor, enalapril] in reducing microalbuminuria. DESIGN: A multinational, multicentre, controlled, double-blind, double-dummy, randomized, two-parallel-groups study over 1 year. METHODS: After a 4-week placebo run-in period, 570 patients (ages 60.0 +/- 9.9 years, 64% men) with type 2 diabetes, essential hypertension [systolic blood pressure (SBP) 140-180 mmHg, and diastolic blood pressure (DBP) < 110 mmHg], and persistent microalbuminuria (20-200 microg/min) were allocated randomly to groups to receive indapamide SR 1.5 mg (n = 284) or enalapril 10 mg (n = 286) once a day. Amlodipine, atenolol, or both were added, if necessary, to achieve the target blood pressure of 140/85 mmHg. RESULTS: There was a significant reduction in the urinary albumin : creatinine ratio. Mean reductions were 35% [95% confidence interval (CI) 24 to 43] and 39% (95% CI 30 to 47%) in the indapamide SR and enalapril groups, respectively. Equivalence was demonstrated between the two groups [1.08 (95% CI 0.89 to 1.31%); P = 0.01]. The reductions in mean arterial pressure (MAP) were 16.6 +/- 9.0 mmHg for the indapamide SR group and 15.0 +/- 9.1 mmHg for the enalapril group (NS); the reduction in SBP was significantly greater (P = 0.0245 ) with indapamide SR. More than 50% of patients in each group required additional antihypertensive therapy, with no differences between groups. Both treatments were well tolerated. CONCLUSIONS: Indapamide-SR-based therapy is equivalent to enalapril-based therapy in reducing microalbuminuria with effective blood pressure reduction in patients with hypertension and type 2 diabetes.

Aged↗
PubMed2005

An overview of the pharmacology and clinical efficacy of indapamide sustained release.

The relationship between blood pressure (BP) and cardiovascular risk is clearly established; hypertension increases the rate of cardiovascular. High systolic blood pressure (SBP) may be the main parameter involved in cardiovascular morbidity and mortality. The benefit of lowering BP, particularly with diuretics has been proven in many outcome studies. Indapamide, a thiazide-type diuretic, was available for many years at a dosage of 2.5 mg in an immediate release formulation. A new sustained release (SR) formulation has been developed in order to allow the same antihypertensive efficacy with a better acceptability profile. This paper reviews the pharmacology of indapamide 1.5 mg SR from the bench to the bedside. Indapamide has a dual mechanism of action: diuretic effect at the level of the distal tubule in the kidney and a direct vascular effect, both of which contribute to the antihypertensive efficacy of the drug. The SR formulation contains a hydrophilic matrix, which delivers a smoother pharmacokinetic profile. This avoids unnecessary plasma peak concentrations, which may be associated with side effects. Indapamide SR has now been extensively used in hypertensive patients, including those at increased risk, for example elderly or diabetic patients. It has been shown to decrease BP, particularly SBP, with 24-h efficacy, allowing a once-daily dosage. Studies have demonstrated BP lowering to be at least as effective as all major therapeutic classes including the more recent antihypertensive drugs. Beyond BP decrease, indapamide SR has also been shown to protect against hypertensive target-organ damage in the heart and the kidney and to have a favorable metabolic profile. A broad evidence-base has accumulated to support the benefit of indapamide 1.5 mg SR in hypertensive patients, alone or as part of combination therapy, as recommended by the majority of guidelines.

Albuminuria↗
PubMed1981

Correction of altered noradrenaline reactivity in essential hypertension by indapamide.

Fourteen patients with untreated mild to moderate essential hypertension had on average an abnormally high cardiovascular reactivity to exogenous noradrenaline and angiotension II, while plasma noradrenaline, renin activity, exchangeable body sodium, and blood volume were normal. Treatment with a low dose of indapamide (2.5 mg/day) for six weeks decreased blood pressure by 10% in these hypertensive patients but not in 13 normal control subjects. Plasma or blood volume and exchangeable sodium were not changed significantly; nevertheless, the latter, and body weight, tended to be decreased slightly. Though a mild reduction in extracellular sodium in both normal and hypertensive subjects appears possible, it may not per se fully explain indapamide's blood pressure-lowering effect in essential hypertension. Indapamide induced a mild decrease in angiotensin II pressor responsiveness in normal or hypertensive subjects, but a possible depressor influence from this change was probably antagonised by a concomitant pronounced increase in plasma renin activity. In hypertensive patients, the abnormally high noradrenaline reactivity was corrected by indapamide without an accompanying increase in endogenous plasma noradrenaline levels. Indapamide-induced changes in blood pressure correlated with those in noradrenaline pressor dose. It was concluded, therefore, that indapamide may decrease blood pressure in essential hypertension at least in part by lowering an abnormally high cardiovascular noradrenaline reactivity without causing an equivalent increase in adrenergic nervous activity.

Adolescent↗
PubMedDate not supplied

A review of 10 years of experience with indapamide as an antihypertensive agent.

Indapamide is an effective antihypertensive agent for which a dual mechanism of action has been put forward: a limited diuretic activity combined with antivasoconstrictive effects, resulting in decreased peripheral vascular resistance. Results from clinical trials show that 2.5 mg indapamide once daily effectively reduces arterial blood pressure in about two-thirds of patients with mild to moderate hypertension and that this reduction is related to the severity of the hypertension. As a rule, indapamide's blood pressure-reducing effect is rapid in onset (within 1 or 2 weeks) and by 1 month reaches 65% of its maximum, which occurs after 3 to 4 months of treatment. No tachyphylaxis has been observed during long-term treatment, nor has withdrawal syndrome at discontinuation of therapy. Indapamide has been successfully combined with beta blockers, methyldopa, and other antihypertensive agents, adding considerable effectiveness without noticeable increase in adverse reactions. In general, the drug is well tolerated and side effects are mild and rare. Possibly in relation to its limited diuretic activity at 2.5 mg daily, long-term treatment seldom elicits significant changes in electrolyte balance. In addition, indapamide does not induce deleterious effects on carbohydrate and lipid metabolism. Indapamide is an effective, well-tolerated, first-line antihypertensive agent. The fact that long-term administration does not induce biochemical abnormalities that constitute cardiovascular risk factors indicates another advantage of the drug.

Aged↗
PubMed1975

A comparative study of the activity of a new agent, indapamide, in essential arterial hypertension.

A single-blind crossover trial was carried out in 38 elderly, hospitalised patients with essential hypertension to compare the hypotensive activity of 5 mg. indapamide daily with 100 mg. chlorthalidone daily. After initial treatment for 10 days with placebo, patients received treatment for 45 days with either indapamide or chlorthalidone and were then crossed over to the alternative drug for a similar period. Potassium supplementation was necessary in 25 of the patients receiving chlorthalidone, but was precribed as a precautionary measure in only 1 patients whilst on indapamide. Results showed that there were significant drops in blood pressure following both active medications, but that the percentage reduction in diastolic pressure was greater after indapamide. Indapamide also proved more effective than chlorthalidone in controlling the patients' subjective and functional symptoms of their hypertension. In an overall assessment of the effectiveness of both drugs, indapamide was judged to be better tolerated as well as more effective than chlorthalidone in 18 of the 38 patients, whilst chlorthalidone was preferred in only 7 instances.

Aged↗
PubMed1983

Correction of altered noradrenaline reactivity in essential hypertension by indapamide.

Fourteen patients with untreated mild to moderate essential hypertension had, on average, an abnormally high cardiovascular reactivity to exogenous noradrenaline and angiotensin II, while plasma noradrenaline, renin activity, exchangeable body sodium, and blood volume were normal. Treatment with a low dose of indapamide (2.5 mg/day) for 6 weeks decreased blood pressure by 10% in these hypertensive patients but not in 13 normal control subjects. Plasma or blood volume and exchangeable sodium were not changed significantly; nevertheless, the latter, and body weight, tended to be decreased slightly. Though a mild reduction in extracellular sodium in both normal and hypertensive subjects appears possible, it may not fully explain per se the blood pressure-lowering effect of indapamide in essential hypertension. Indapamide induced a mild decrease in angiotensin II pressor responsiveness in normal or hypertensive subjects, but a possible depressor influence from this change was probably antagonized by a concomitant pronounced increase in plasma renin activity. In hypertensive patients, the abnormally high noradrenaline reactivity was corrected by indapamide without an accompanying increase in endogenous plasma noradrenaline levels. Indapamide-induced changes in blood pressure correlated with those in noradrenaline pressor dose. It was concluded, therefore, that indapamide may decrease blood pressure in essential hypertension at least in part by lowering an abnormally high cardiovascular noradrenaline reactivity without causing an equivalent increase in adrenergic nervous activity.

Adolescent↗
PubMed2004

Effects of a low dose of indapamide, a diuretic, given daily or every-other-day on blood pressure and metabolic parameters.

To investigate the effects of the diuretic, indapamide, on blood pressure (BP) and metabolic parameters, thirty hypertensive patients were treated with 1 mg of indapamide either every day or every other day. BP, fasting plasma glucose, lipids, serum potassium and uric acid were determined at baseline and after 3 months of a stable regimen of the drug. At the termination of the study, 48-h ambulatory blood pressure monitoring (ABPM) was performed. Three patients received only indapamide, while other patients were treated in combination with additional antihypertensive medications. Patients treated with daily indapamide showed a BP reduction from 162 +/- 2.9/85 +/- 2.4 mmHg to 134 +/- 2.4/71 +/-2.6 mmHg (p < 0.001). The BP reduction was similar in those patients receiving the drug every other day (137 +/- 3.4/71 +/- 3.6 mmHg). While plasma lipids and serum potassium did not differ significantly with the intervention, uric acid increased significantly with daily treatment and normalized with every-other-day treatment. Glycosylated hemoglobin A1c (HbA1c) was not altered (5.6 +/- 0.1% vs. 5.4 +/- 0.2%), and did not differ between patients with and without diabetes mellitus. ABPM revealed an average 24-h BP of 134 +/- 3.3/75 +/- 1.7 mmHg on days in which patients received the medication and 139 +/- 4.9/78 +/- 2.6 mmHg on the intervening day without indapamide (no significant difference). These results suggest that a low dose of indapamide given every day or every other day is effective in lowering BP and does not result in metabolic derangements.

Aged↗
PubMed2005

Effect of indapamide on urinary calcium excretion in patients with and without urinary stone disease.

BACKGROUND: Indapamide is an antihypertensive agent similar to thiazides, but with some different effects. Thiazide and thiazide-like diuretics are useful in preventing recurrent urinary stone formation due to their hypocalciuric effects. OBJECTIVE: To determine the hypocalciuric and other effects on certain laboratory parameters of indapamide 1.5 mg in different patient groups. METHODS: Four groups of patients recruited from urology and nephrology outpatient departments were experiencing non-hypercalciuric urinary stone disease (group 1), idiopathic hypercalciuria (group 2), urinary stone disease with hypercalciuria (group 3), and essential hypertension (group 4). In all patients, fasting serum uric acid, calcium, sodium, potassium, cholesterol, triglyceride, parathyroid hormone (PTH) values, and morning second-spot urine calcium and creatinine levels were assessed before and 8 weeks after treatment with indapamide. RESULTS: Urinary calcium excretion was reduced significantly in all groups: group 1 from 0.10 +/- 0.02 to 0.07 +/- 0.03 (mean +/-SD; 30% reduction; p < 0.001), group 2 from 0.30 +/- 0.15 to 0.15 +/- 0.10 (50% reduction; p < 0.001), group 3 from 0.35 +/- 0.15 to 0.20 +/- 0.10 (43% reduction; p < 0.001), and group 4 from 0.10 +/- 0.03 to 0.08 +/- 0.02 (20% reduction; p < 0.0010). These results should be interpreted with caution since no control group was included in this study. Mean serum uric acid and triglyceride levels were significantly increased, and mean PTH and potassium levels and diastolic and systolic blood pressure were significantly decreased in all groups. Few temporary adverse effects, such as dizziness and fatigue, were noticed and none of them caused discontinuation of treatment. CONCLUSIONS: Indapamide 1.5 mg/day is effective in decreasing calciuria in patients with non-hypercalciuric urinary stone disease, idiopathic hypercalciuria, urinary stone disease with hypercalciuria, and essential hypertension. This could be achieved with few adverse effects similar to those of thiazides and indapamide 2.5 mg. Indapamide decreased the PTH levels in all groups. Long-term clinical benefits of these effects should be evaluated prospectively with further randomized studies.

Adult↗
PubMed1999

Perindopril + indapamide: new preparation. Simple trick.

(1) The combination of perindopril 4 mg + indapamide 1.25 mg is approved for second-line treatment of hypertension after failure of perindopril alone. (2) The other combination, of a low dose of an angiotensin-converting-enzyme inhibitor (2 mg of perindopril) and a diuretic (0.625 mg of indapamide), is being promoted as first-line treatment of hypertension. (3) The clinical files for both preparations are limited to the strict minimum. (4) A dose-finding study showed that the perindopril 4 mg + indapamide 1.25 mg dose combination offered the best risk-benefit ratio by comparison with combinations containing the same perindopril dose but other indapamide doses. (5) A double-blind trial suggests that the antihypertensive activity of the perindopril 4 mg + indapamide 1.25 mg combination is equivalent to that of the captopril 50 mg + hydrochlorothiazide 25 mg and enalapril 20 mg + hydrochlorothiazide 12.5 mg combinations. The safety profile was the same for the three combinations. (6) The 2-mg perindopril combination has not been compared with perindopril monotherapy at the usual dose of 4 mg, or with indapamide monotherapy at a mean dose of 2.5 mg. (7) The two combinations are costlier than their competitors.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

[Comparative assessment of hypotensive, metabolic, and endothelial effects of indapamide-retard and hydrochlorothiazide in patients with essential hypertension].

AIM: To compare hypotensive, metabolic, and endothelial effects of indapamide-retard and hydrochlorothiazide. MATERIAL AND METHODS: Patients (n=50) with essential hypertension were given either indapamide-retard (1.5 mg/day, n=25) or hydrochlorothiazide (25 mg/day, n=25) for 12 weeks. Dynamics of the following parameters were studied: blood pressure, blood lipids and glucose, total coronary risk, carotid artery intima-media thickness, reaction of brachial artery to endothelium-dependent and endothelium-independent stimuli registered by high resolution ultrasound. RESULTS: Indapamide-retard and hydrochlorothiazide demonstrated similar hypotensive efficacy. Indapamide-retard turned out to be metabolically neutral while in patients receiving hydrochlorothiazide we observed significant elevation of triglycerides (+15.3%, p<0.05) and glucose (+12.2%, p<0.05). This resulted in the lack of lowering of total coronary risk during treatment with hydrochlorothiazide. Significant intergroup differences were revealed in effects on endothelium-dependent vasodilation with tendency to improvement and to significant worsening (-17%, p<0.05) in indapamide and hydrochlorothiazide treated patients, respectively. CONCLUSION: Despite similar hypotensive efficacy there were significant differences in metabolic and endothelial effects of 2 diuretics in favor of indapamide. This could potentially matter for long term cardiovascular prognosis.

Aged↗
PubMed2006

Effects of valsartan and indapamide on plasma cytokines in essential hypertension.

OBJECTIVE: investigate and compare the effect of valsartan and indapamide on inflammatory cytokines in hypertension. METHODS: Forty-one untreated patients with mild to moderate hypertension and 20 age and sex-matched normotensives were enrolled in this study. Hypertensives were treated with indapamide 1.5 mg/d (n=20) or valsartan 80 mg/d (n=21) for 4 weeks, and blood samples for determining monocyte chemotactic protein-1 (MCP-1), macrophage inflammatory protein-1 (MIP-1alpha), sP-selectin, asymmetric dimethylarginin (ADMA), angiotensin II (Ang II), and 6-keto-PGF1alpha were collected before the treatment and 4 weeks after the treatment. RESULTS: Hypertensives exhibited significantly higher blood pressure, as well as elevated plasma levels of MCP-1, MIP-1alpha, sP-selectin and serum level of ADMA compared with the normotensives. Nevertheless, there was no significant difference in serum 6-keto-PGF1alpha and Ang II between the hypertensives and the normotensives. After the treatment with indapamide or valsartan for 4 weeks, both the systolic and diastolic blood pressures, though still higher than those of the normotensives, decreased markedly. After the treatment with indapamide for 4 weeks, MCP-1, MIP-1alpha and sP-selectin slightly decreased, but not statistically significant (P>0.05). Those cytokines decreased significantly after being treated with valsartan for 4 weeks [(19.16+/-3.11) pg/mL vs (16.08+/-2.67) pg/mL, P<0.05; (27.74+/-8.36) pg/mL vs (17.64+/-7.59) pg/mL, P<0.05; (2.67+/-3.18) pg/mL vs (6.15+/-2.94) pg/mL, P<0.01]. In the 2 treatment groups, 6-keto-PGF1alpha markedly increased [(61.96+/-20.81) pg/mL vs (96.72+/-25.89) pg/mL, P<0.05; (63.25+/-16.92) pg/mL vs (143.22+/-43.45) pg/mL, P<0.01]; ADMA decreased significantly [(1.35+/-0.74) pg/mL vs (0.98+/-0.56) micromol/L, P<0.05; (1.31+/-0.68) pg/mL vs (0.71+/-0.52) micromol/L, P<0.01]. Though Ang II slightly increased, no statistical significance was found (P>0.05). CONCLUSION: The levels of MCP-1, MIP-1alpha, sP-selectin and ADMA were elevated in mild to moderate hypertensives. Valsartan and indapamide have similar blood pressure lowering effect. Valasartan exerts more significant effect on cytokines than indapamide does.

Adult↗