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PubMed2000

Indapamide blocks the rapid component of the delayed rectifier current in atrial tumor cells (AT-1 cells).

We studied the effects of a well known blocker (indapamide) of the slow component (I(ks)) of the delayed rectifier (I(k)) on K(+) currents in atrial tumor myocytes derived from transgenic mice (AT-1 cells) using one electrode voltage clamp method. These cells have been shown to express mRNAs encoding cardiac K(+) channels and display a cardiac electrophysiological phenotype. The major K(+) current is the rapid component (I(kr)) of the delayed rectifier current (I(k)). The purpose of this study was to show that a diuretic agent, indapamide, which was shown to be a selective blocker of the slow component (I(ks)) of delayed rectifier, also blocks I(kr) in a dose dependent manner. The steady state current at the end of a 1s pulse (I(1s), step to +40 mV from a holding potential of -40 mV) was 1070.4+/-202.2 pA (n=5) and the tail current (I(tail)) was 416.3+/-112.9 pA. Indapamide (750 microM) reduced I(1s) and I(tail) to 254.5+/-62.3 pA and 42.2+/-37.7 pA respectively. Indapamide induced block was partially reversible for higher concentrations (> or =750 microM).

Action Potentials↗
PubMed2001

Stripping voltammetric determination of indapamide in serum at castor oil-based carbon paste electrodes.

The diuretic drug indapamide has been characterized voltammetrically at carbon paste electrodes by means of cyclic and differential pulse voltammetry. An adsorptive stripping method at carbon paste electrode modified with castor oil for trace determination of indapamide was described. A study of the variation of the peak current with solution variables such as pH, ionic strength, concentration of indapamide, possible interference, and instrumental variables such as scan rate, pulse amplitude, preconcentration time, accumulation potential, paste composition has resulted in the optimization of the oxidation signal for analytical purposes. By anodic stripping differential pulse voltammetry, the calibration plot was linear in the range 5 x 10(-8) x 10(-7) M with a detection limit of 5 x 10(-9) M at carbon paste electrode modified with castor oil in pH 4.0. The preconcentration medium-exchange approach was utilized for selective determination of indapamide in spiked serum. A detection limit of 15 ng ml(-1) was obtained for dilute serum sample after 3 min accumulation and medium-exchange procedure.

Carbon↗
PubMed1992

Beneficial effect of indapamide in experimental myocardial ischemia.

Indapamide, a nonthiazide chlorosulfamoyl diuretic, which possesses well-known antihypertensive properties, is able to scavenge free radical intermediates involved in lipid peroxidation. In this respect, it has almost the same level of action as alpha-tocopherol. Using an isolated working rat heart preparation, we investigated the effect of indapamide on the myocardial resistance to global total normothermic ischemia followed by reperfusion. The heart, isolated at the end of chronic oral pretreatment (7 day at 3 mg/kg body weight/day), was submitted to ischemia for 15 min and then reperfused. The main results were as follows: in the indapamide-treated group, 1) postischemic recovery of cardiac function was significantly better as compared to the untreated control group; 2) lactate dehydrogenase (LDH) release measured after 15 min of reperfusion was significantly reduced; 3) the myocardial content of organic hydroperoxides (HPO), taken as an index of lipid peroxidation, was significantly lowered, whereas the activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx) remained unchanged; and 4) electron spin resonance (ESR) analysis of coronary effluents, collected during the first minutes of reperfusion in the presence of the spin-trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO), revealed a significant modification in the treated group. These findings suggest that indapamide treatment is able to afford some protective effect to cardiac tissue during the early stage of postischemic reperfusion, and that this effect might be related to the antioxidant properties of inadapamide.

Animals↗
PubMed1989

Hypertension and micro-albuminuria in diabetic patients taking indapamide.

The effects of indapamide on diabetic patients with micro-albuminuria were evaluated in a multicentre study to assess the advantages of this compound in long-term renal protection. Thirty-two hypertensive diabetic patients (10 males, 22 females, aged 46-84 years) were given indapamide at 2.5 mg/day for a 2-month period. There was a significant fall in systolic blood pressure (174 +/- 18 to 148 +/- 12 mmHg, P less than 0.001) and diastolic blood pressure (95 +/- 13 to 85 +/- 8 mmHg, P less than 0.001) and in the albumin excretion rate (median, 40.8 to 18.9 mg/l; P less than 0.05). Blood glucose, glycosylated haemoglobin, electrolytes, creatinine and serum lipids remained unchanged. There was a small but significant correlation between changes in systolic blood pressure and changes in albuminuria (r = 0.04, P less than 0.05). Thus, the effect of indapamide on albumin excretion cannot be explained by a decrease in the intraglomerular perfusion pressure alone. Indapamide, therefore, might be of potential interest in the long-term renal protection of the diabetic patient with elevated blood pressure values and/or micro-albuminuria.

Aged↗
PubMed1981

Indapamide and bendrofluazide: a comparison in the management of essential hypertension.

1 To compare the efficacy of indapamide with that of bendrofluazide a randomised trial was carried out in twenty patients with essential hypertension. 2 Indapamide (2.5 mg a day) and bendrofluazide (5 mg a day) produced a significant but equivalent fall in blood pressure. 3 Both drugs caused a reduction in body weight and serum potassium with a rise in plasma renin activity but there were no other major side effects. 4 In twelve patients treated with a combination of indapamide and bendrofluazide there was no additional fall in mean blood pressure or serum potassium compared to treatment with bendrofluazide or indapamide alone.

Adult↗
PubMed2002

Very-low-dose combination of the angiotensin-converting enzyme inhibitor perindopril and the diuretic indapamide induces an early and sustained increase in neovascularization in rat ischemic legs.

After acute ischemia of tissues, neovascularization must be sufficient and fast enough to preserve tissue integrity and organ function, and may thus be considered as a therapeutic strategy. This study examined the possible role of the very-low-dose combination of perindopril (angiotensin-converting enzyme inhibitor) and indapamide (diuretic), used first-line in the treatment of essential hypertension, on ischemia-induced angiogenesis. Ischemia was produced by artery femoral occlusion in rats treated or not with the very-low-dose combination (perindopril 0.76 mg/kg/day + indapamide 0.24 mg/kg/day) or each component given alone at the same dosage for 3 and 28 days. At day 3, angiographic vessel density and laser Doppler perfusion data showed significant improvement in ischemic/nonischemic leg ratio by, respectively, 1.9-fold and 1.5-fold in rats treated with the very-low-dose combination when compared with controls (p < 0.05). This was associated with an increase in vascular endothelial growth factor (VEGF; 2.2-fold) and endothelial nitric-oxide synthase (1.6-fold) protein content in the ischemic hindlimb, assessed by Western blot. At day 28, the very-low-dose combination (3- and 1.6-fold) and perindopril alone (1.8- and 1.4-fold) and indapamide alone (2.0- and 1.4-fold) increased the angiograhic score and blood flow perfusion, respectively, in reference to controls (p < 0.05). Furthermore, addition of VEGF-neutralizing antibody (2.5 microg/kg twice a week) or NOS inhibitor (N(G)-nitro-L-arginine methyl ester, 10 mg/kg/day) prevented the pro-angiogenic effect induced by the perindopril/indapamide combination. The very-low-dose combination of perindopril and indapamide induces an early and sustained effect on the revascularization process observed in ischemic tissue and may provide a favorable therapeutic neovascularization after ischemia.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2005

[Utility of extended release indapamide in the treatment of hypertension in at risk elderly: extended release study].

INTRODUCTION: It is estimated that more than 65% of the elderly population in Spain is hypertensive. This study aimed to evaluate the safety and efficacy of extended release indapamide in hypertensive patients over 60 years of age, having high cardiovascular risk and the factors that influence this effect. MATERIAL AND METHODS: Prospective study made in 944 patients with essential HBP and age > 60 years (55.9% women) in whom treatment with extended release indapamide in single drug therapy or in combination was indicated, whether as a new drug or due to lack of efficacy of the previous therapy. The action scope was hospital out-patient clinics of Internal Medicine and follow-up time of the patients was 6 months. RESULTS: Extended release indapamide causes a significant decrease (p < 0.05) of systolic blood pressure (SBP) (21.3 mmHg) and diastolic blood pressure (DBP) (10.8 mmHg). No significant differences were found between the results in monotherapy or combined therapy. A total of 52.7% of the patients included had 3 or more cardiovascular risk factors (RF) or had target organ lesion (TOL) and 41.1% had an associated cardiovascular disease (CVD). Those patients with greater baseline SBP and DBP were those having a greater decrease in BP. On the other hand, patients with 1 or 2 RF showed a greater decrease of the SBP in comparison with patients with 3 or more RF, TOL or associated CVD. The adverse reactions rate was 2.8%. CONCLUSIONS: Extended release indapamide is an effective drug in the elderly population having high cardiovascular risk and is well tolerated.

Aged↗
PubMed1988

Acute effect of indapamide on urine calcium excretion in nephrolithiasis and human essential hypertension.

The effects of indapamide (2.5 mg once a day) on urinary composition are reported in 20 patients (10 with recurrent calcium nephrolithiasis and 10 with essential hypertension) compared with 20 controls. Indapamide was well absorbed in every patient (mean plasma level at the steady state was 111 +/- 41 ng/ml) and its antihypertensive action was more pronounced in hypertensive than in normotensive patients. It lowered calcium excretion in 18/20 patients (mean fall on the 7th day of treatment: 53%) and raised the Mg/Ca ratio in 20/20 patients (mean increase on the 7th day: 167%). The effect on Ca2+ and Mg2+ excretion was not associated with a strong diuretic effect. During intravenous calcium loading (0.375 mmol/kg body weight) 6 normal subjects after a single oral dose of indapamide excreted less calcium, suggesting a direct renal hypocalciuric action by the drug. Indapamide could represent an alternative drug to thiazide diuretics in diseases with dangerous renal calcium losses, but long-term studies are needed.

Adult↗
PubMed1983

The possible mode of action of indapamide: a review.

It is not clear whether indapamide reduces blood pressure by a vasodilator or a diuretic action. This review attempts to answer this fundamental question. Cardiovascular studies show small increases in cardiac output, heart rate and stroke volume with a significant reduction in peripheral resistance. Indapamide, in vitro, directly inhibits pressor stimuli probably through a reduction of calcium flux in vascular smooth muscle, whilst diuretics are inactive. In vivo studies in man also show a reduction in sensitivity to pressor doses of noradrenaline and angiotensin without an increase in adrenergic sensitivity. However, indapamide does have mild diuretic activity at therapeutic doses, as shown by changes in plasma sodium, potassium, urea, uric acid and a reduction in body weight, but the changes are appreciably less than with thiazides. These results would suggest that indapamide has both diuretic and vasodilator properties. A low urinary excretion and specific accumulation into arterial smooth muscle of this lipophilic molecule may provide a rationale for this dual activity.

Benzothiadiazines↗
PubMed1986

Antihypertensive effect of indapamide given in conjunction with captopril in severe hypertension.

The efficacy of captopril alone or in combination with indapamide was evaluated in 17 patients with severe hypertension (diastolic greater than 120 mmHg) previously treated with triple antihypertensive therapy, i.e. diuretic, beta-blocker and a vasodilator. After a wash-out period of 1 week, captopril was given initially as 75 mg/day for 2 weeks; at the end of this period, the dosage was doubled to 150 mg/day and continued at this level for a further 2 weeks. Indapamide (2.5 mg/day) was then added to the regimen and administered for 1 month. The results showed that captopril alone lowered, but did not normalize the blood pressure. The mean diastolic pressure was reduced to 117 and 103.8 mmHg after dosages of captopril of 75 mg and 150 mg, respectively. On the addition of indapamide, the blood pressure was normalized to 93.82 mmHg mean diastolic pressure. Systolic readings were similarly reduced. Two patients developed skin rashes while on captopril alone: no other treatment-related side-effects were reported once indapamide therapy had commenced.

Blood Pressure↗
PubMed1991

Effect of indapamide on the proliferation of Balb/C 3T3 cells induced by platelet-derived growth factor.

The effects of indapamide (a nonthiazide antihypertensive diuretic) on the growth promoting activity of serum, platelet-derived growth factor (PDGF), fibroblast growth factor (FGF) or Ca3(PO4)2 on Balb/C 3T3 cells were studied. Indapamide inhibited the growth promoting activity of serum, but furosemide (a nonthiazide antihypertensive diuretic) had no such inhibitory effect. Indapamide inhibited the growth promoting activity of PDGF, but not that of FGF and Ca3(PO4)2. The present experiments demonstrate that indapamide selectively inhibits the growth promoting activity of PDGF.

3T3 Cells↗
PubMed1985

Double-blind comparison of indapamide with a placebo in hypertensive patients treated by practicing physicians.

The antihypertensive effect of indapamide (2.5 mg/day) was compared to that obtained with a placebo in a controlled trial carried out by 11 physicians in their private practice. Thirty-one patients with uncomplicated essential hypertension were included. After a run-in period of 3 weeks without any treatment, either indapamide (n = 16) or a placebo (n = 15) were administered for 8 weeks in double-blind fashion. Blood pressure decreased in both groups. In patients treated with indapamide, systolic pressure was significantly lower than in those given the placebo at 3 out of the 4 follow-up visits; diastolic pressure, however, was significantly lower only at the end of the trial. Both the active drug and the placebo were well tolerated. No significant change in body weight, plasma potassium and uric acid occurred during the study in either group of patients. It appears therefore that indapamide, at a dose which apparently has no major diuretic effect, may be useful for practitioners in managing patients with mild to moderate hypertension.

Adult↗
PubMed2000

Effects of indapamide versus hydrochlorothiazide on plasma lipids and lipoproteins in hypertensive patients: a direct comparison.

To test the claim that indapamide causes fewer adverse metabolic effects than hydrochlorothiazide (HCTZ), six months of treatment with HCTZ 25 mg/day was compared with six months of treatment with indapamide 2.5 mg in a randomized double-blind study of 44 patients with mild to moderate hypertension. Both drugs significantly reduced blood pressure, with no significant differences in the reduction of potassium and chloride; neither drug was associated with a significant change in plasma total cholesterol, high density lipoprotein (HDL), apolipoprotein A1, apolipoprotein B or the ratio of total cholesterol to HDL levels. Triglyceride levels increased significantly more with indapamide than with HCTZ (P=0.02). The two drugs had similar effects on blood pressure and serum potassium; neither drug affected plasma glucose. Claims that indapamide is superior to HCTZ appear unwarranted; in view of the substantial cost difference, this finding, if confirmed in larger studies, has important policy implications.

Adolescent↗
PubMed1999

[Study on the antidiuretic efficacy and mechanism of indapamide in central diabetes insipidus].

OBJECTIVE: To investigate the efficacy and antidiuretic mechanism of indapamide in central diabetes insipidus. METHODS: We observed eight patients with central diabetes insipidus treated by indapamide (2.5-7.5 mg.d-1) or dihydro-chlorothiazide (50-70 mg.d-1) or carbamazepine (150-300 mg.d-1) for 8 days with randomized block design. The therapy was changed twice in sequence after 4 days without treatment. Urine output and indexes of water metabolism were also observed. RESULTS: The urine output was reduced on the 4th day and 8th day with each therapy. The serum potassium and chloride concentration was decreased and renin activity was increased on the 4th and 8th day with indapamide therapy. CONCLUSION: Indapamide has antidiuretic action on central diabetes insipidus. The action may result from the changes of hydroelectrolytes and renin-angiotensin-aldosterone system.

Adolescent↗
PubMed1992

[The effect of indapamide on plasma prostaglandins in hypertensive patients].

After two weeks' treatment of indapamide (2.5 mg/d) in 30 cases of mild to moderate hypertensive patients, there was a significant decline of systolic and diastolic blood pressure. And 8 weeks after indapamide administration, 2/3 of the total treated patients achieved complete control of hypertension. During the treatment period, there were no changes of serum cholesterol, triglyceride and renal function, except a slight, but still in the normal range, decrease of serum potassium and sodium. Concurrently, plasma vasoconstrictive prostaglandins TXB2 (metabolite of TXA2) and PGF2 alpha reduced significantly (P < 0.01 and P < 0.001 respectively), whereas plasma vasodilative prostaglandins 6-keto-PGF1 alpha (metabolite of PGI2) and PGE2 increased significantly (P < 0.02 and P < 0.05 respectively). The results support the theory that prostaglandins system may play an important role in the hypotensive process of indapamide. The influence of indapamide on prostaglandin system may favour the improvement of platelet function and the maintenance of the homeostasis.

Adult↗
PubMed2005

Rapid and sensitive determination of indapamide in human blood by liquid chromatography with electrospray ionization mass spectrometric detection: application to a bioequivalence study.

A rapid and sensitive method using liquid chromatography with electrospray ionization mass spectrometric detection was developed and validated for the determination of indapamide in human blood. Blood samples were extracted with n-hexane-dichloromethane (1:1, v/v) and separation was performed on a Symmetry C18 column (150 x 3.9 mm i.d., 5 microm) with the mobile phase consisting of acetonitrile-water (60:40, v/v). Indapamide and internal standard (propylparaben) were detected by negative electrospray ionization and selected ion recording (SIR) at m/z 364 for indapamide and m/z 179 for propylparaben. This method has a lower limit of quantification (LLOQ) 2.0 microg/L with a linear calibration range of 2.0 microg/L to 120 microg/L. The method showed excellent reproducibility with an inter- and intra-assay precision of < 9.4% (% RSD), as well as excellent accuracy with an inter- and intra-assay accuracy of between 98.0 and 102%. Furthermore, the method was successfully applied to a bioequivalence study in which 20 healthy volunteers received a single oral dose of 3 mg reference and test sustained-release indapamide formulations, in an open, two-period, randomized crossover protocol. The maximum blood concentrations (C(max)) were 60.3 +/- 22.6 microg/L and 57.6 +/- 18.7 microg/L at 13.1 +/- 6.9 h and 18.3 +/- 7.4 h, the times to reach the peak concentration (T(max)), for the test and reference tablets, respectively. The relative bioavailability of the test tablets was 110.1 +/- 34.5%, compared with the reference tablets. There were no statistically significant differences in the main pharmacokinetic parameters, and the two formulations were judged to be bioequivalent.

Antihypertensive Agents↗
PubMed2006

[Use of spironolactone and indapamide in the treatment of low-renin arterial hypertension].

AIM: To compare efficacy of use of the blocker of aldosteron receptors spironolactone and diuretic indapamide in low-renin arterial hypertension (AH), their action on blood pressure, serum concentrations of sodium, potassium, creatinine, plasmic renin activity (PRA), plasmic aldosteron concentration (PAC). MATERIAL AND METHODS: The study included 31 females aged 40-60 years with hardly correctable AH and high PAC to (PRA) ratio. Biochemical parameters were measured before 2-week treatment with indapamide (1.5 mg/day) and spironolactone (25 mg/day) and after the treatment. Between the courses there was a 2-week interval. RESULTS: In AH patients with high PAC/PRA spironolacton reduced AP more significantly (-15.5 / -8.2 mmHg) than indapamide (-10.9 / -5.9 mmHg). Indapamide lowered potassium serum levels by 0.28 mmol/l (p < 0.05), spironolacton raised it by 0.26 mmol/l (p = 0.05). Sodium concentration in the serum reduced only after treatment with spironolactone. Both drugs increased blood concentrations of creatinine, aldosteron, PRA, but spironolactone was more active. CONCLUSION: In treatment-resistant AH it is necessary to perform screening for detection of patients with low-renin hypertension. Such patients are effectively treated with spironolacton in low doses.

Adult↗
PubMed1988

Indapamide-induced inhibition of calcium movement in smooth muscles.

The effects of indapamide on ionic currents and isometric contractions in both rat myometrium and rat portal vein preparations were studied. Indapamide (3 x 10(-4) M) depressed both inward calcium and outward potassium currents. The decrease in potassium current was dependent on the reduction of the inward calcium current. Indapamide reduced the transient contraction induced in calcium-free, ethylene glycol-bis(B-aminoethylether)-N,N'tetra-acetic acid-containing solutions by either acetylcholine (10(-4) M) or norepinephrine (10(-5) M). The results indicate that indapamide acts primarily on the plasma membrane of spontaneously active smooth muscles by reducing the calcium current; it may also depress contractions supported by release of calcium from the sarcoplasmic reticulum.

Animals↗