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PubMed1986

Effect of indapamide on the electromechanical properties of rat myometrium and rat portal vein.

The effects of indapamide were studied on membrane potentials, ionic currents and isometric contractions in pregnant rat uterine smooth muscle. Indapamide (5 X 10(-6) to 10(-3) M) depressed K contractures and twitch contractions within 3 to 6 min. At a concentration of 3 X 10(-4) M, indapamide decreased the rate of rise, amplitude and rate of repolarization of the action potential and prolonged the potential duration. The inward current, carried either by Ca or Na ions, was depressed without modification of the respective reversal potentials. The decrease in K outward current was dependent on the reduction of the Ca inward current. In both myometrium and rat portal vein, indapamide depressed the transient contractions induced in Ca-free, ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid-containing solutions by either acetylcholine (10(-4) M) or norepinephrine (10(-6) M). In myometrium, the maintained and repetitive contractions induced by acetylcholine as well as the contractions produced by prolonged membrane depolarizations were not affected by indapamide. The results indicate that indapamide acts primarily on the plasma membrane of spontaneously active smooth muscles by reducing both inward (Ca and Na) currents and outward (K) current; it may also exert an effect to depress contractions supported by a release of Ca from the sarcoplasmic reticulum.

4-Aminopyridine↗
PubMed1988

Effect of indapamide on serum and red cell cations, with and without magnesium supplementation, in subjects with mild hypertension.

Unlike some thiazide diuretics, indapamide--a non-thiazide chlorosulphonamide derivative--has been shown to have a magnesium-sparing effect in normotensive subjects. This effect has not been studied in hypertensive subjects. In a randomised double-blind trial indapamide 2,5 mg and placebo were given daily to a group of elderly patients with mild hypertension, with and without supplemental magnesium chloride. Blood pressure and serum and red blood cell cations were measured. The significant antihypertensive effect of indapamide was confirmed. There was no effect of indapamide on serum and red cell magnesium concentrations compared with placebo, both with and without magnesium supplementation. Indapamide induced hypokalaemia with a shift of sodium into the red cells. In this group of elderly hypertensive subjects indapamide induced potassium but not magnesium loss.

Adult↗
PubMed1985

[Comparative effects of nifedipine and indapamide in the treatment of arterial hypertension].

A controlled multicentre trial was organised to compare the effects of 20 mg Nifedipine tablets (N) and 2,5 mg Indapamide tablets (I) during a 4 months' treatment period after a placebo period, in 59 patients with moderate essential hypertension (n = 59). The results of blood pressure measurements of 18 patients treated by nifedipine (1 tablet twice daily) and 22 patients treated by indapamide (1 tablet every morning) were compared. The systolic blood pressure, after 10 minutes recumbency, fell from 165 +/- 10 mmHg to 148 +/- 13 mmHg (p less than 0.01), and the diastolic pressure from 104 +/- 6 mmHg to 86 +/- 7 mmHg (p less than 0.01) in the patients treated with nifedipine. In the indapamide group, the SBP fell from 164 +/- 13 mmHg to 152 +/- 15 mmHg (p less than 0.01) and the DBP from 100 +/- 4 mmHg to 87 +/- 6 mmHg (p less than 0.01). There were no significant changes of heart rate with either drug; plasma creatinine, potassium and uric acid concentrations were also unchanged. There was a higher incidence of headaches and tiredness in the nifedipine group, whilst patients treated with indapamide complained more often of muscular cramps. Flushing was observed in nearly a quarter of the patients in both groups. These results confirm that both nifedipine and indapamide induce significant and persistant falls in systolic and diastolic blood pressure. Although the fall was greater with nifedipine than with indapamide, the difference was not statistically significant. The tolerance was satisfactory in both groups of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Indapamide: a review.

Indapamide (Natrilix; Servier) is an antihypertensive diuretic which is used at a dose of 2.5 mg/d as first-line single-drug treatment of essential arterial hypertension. Indapamide effectively controls blood pressure in about 65% of cases of mild and moderate hypertension. The time-course of the antihypertensive effect of this drug consists of a clinically significant fall in blood pressure after the 1st week of treatment and of a further reduction that follows a decreasing power function of time thereafter. When an epidemiological approach to the mass treatment of hypertension is considered, the time-course of the antihypertensive effect of indapamide constitutes an advantage over diuretics such as the thiazides that lower blood pressure mildly during the 1st week of treatment and then proceed to lower it in a linear pattern thereafter. Indapamide does not increase magnesium excretion when given in single doses to normal volunteers. This distinguishes it from most diuretic formulations in current use, which increase renal magnesium excretion. The difference could be explained by the fact that the dose of indapamide usually employed is devoid of major diuretic activity although it still exhibits power antihypertensive properties. Since magnesium depletion provoked by diuretics seems to be the principal causative factor in the development of sudden cardiac death in patients under treatment with diuretics, indapamide should be regarded as one of the best options from this point of view.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1983

A systemic hemodynamic evaluation of indapamide.

The hemodynamic effects of indapamide were evaluated in an open clinical trial of nine patients with mild to moderate hypertension. Hemodynamic and echocardiographic measurements were made before and after six weeks of treatment with single daily doses of 2.5 mg of indapamide. Indapamide significantly reduced the mean standing systolic blood pressure (P less than 0.025), the mean standing diastolic blood pressure (P less than 0.01), the mean arterial blood pressure (P less than 0.001), and the mean total peripheral vascular resistance (P less than 0.01). Cardiac output increased 12% (P less than 0.05) during treatment. The heart rate, left ventricular end-diastolic and end-systolic volumes, systolic volume, and ejection fraction were not markedly altered after treatment with indapamide, although the systolic wall stress index fell slightly. Six weeks of indapamide administration was well tolerated with no notable adverse effects of the drug. The results suggest that indapamide reduces arterial blood pressure in hypertensive patients by decreasing total peripheral resistance.

Adult↗
PubMed1980

Cardiovascular effects of indapamide on frog hearts and open-chest cats.

Unlike related diuretics indapamide has been found by some investigators to be associated with a mild reduction in heart rate during its use as an antihypertensive agent. This investigation concerns the attempt to duplicate this phenomenon in animals and to elucidate possible mechanisms. In isolated frog hearts, high concentrations (0.3 mM) of indapamide decreased contractions 21.7 +/- 1.2% and rate 9.1 +/- 1.0%. This effect was not observed with chlorothiazide, acetazolamide, or furosemide and was not altered by atropine. Also in the frog heart, 0.03 mM indapamide reduced the stimulatory effects of isoproterenol and calcium ion and enhanced the inhibitory action of acetylcholine. In open-chest cats, after 30 min, indapamide (3 mg/kg, i.v.) elicited minor decreases in heart rate, aortic flow, and mean carotid pressure. When arterial pressure was rapidly reduced by acetylcholine (5 microgram/kg, i.v.) the resultant rise in aortic flow was significantly diminished by indapamide pre-treatment. Antifibrillatory activity was measured in the open-chest cat by determining the minimum electrical current, delivered to the right atrium, required to induce atrial fibrillation. Quinidine (5 mg/kg, i.v.) and chlorothiazide (10 mg/kg, i.v.) raised the fibrillatory threshold 94.3 +/- 10.1 % and 45.1 +/- 4.0 % respectively while indapamide displayed minimal activity.

Acetylcholine↗
PubMed1995

An equivalence study of the safety and efficacy of a fixed-dose combination of perindopril with indapamide versus fixed-dose combinations of captopril with hydrochlorothiazide and enalapril with hydrochlorothiazide in the treatment of hypertension.

OBJECTIVE: The aim of this multicenter, randomly allocated, double-blind, parallel-group study was to evaluate the equivalence of three fixed-dose combination drugs in mild to moderate hypertension: perindopril + indapamide (4 + 1.25 mg), captopril + hydrochlorothiazide (50 + 25 mg) and enalapril + hydrochlorothiazide (20 + 12.5 mg). PATIENTS AND METHODS: After a single-blind, 4-week, placebo run-in phase, 527 patients (mean +/- SD age 54.5 +/- 1.2 years) with a supine diastolic blood pressure of 101.2-101.7 mmHg were randomly assigned to one of the three treatments for 8 weeks. The main evaluation criteria were diastolic blood pressure and serum potassium concentration. Equivalence was assessed on an intention-to-treat basis, using Schuirmann's method, which involves performing two one-tailed statistical tests on the data. Thirty-five patients were withdrawn from the study but there were no differences between groups in the reasons for withdrawal. RESULTS: Diastolic blood pressure decreased by between 13.1 and 14.2 mmHg in the three groups. The 90% confidence intervals for the differences between perindopril + indapamide and the other treatments were -1.1, +1.7 mmHg for captopril + hydrochlorothiazide and -0.4, +2.6 mmHg for enalapril + hydrochlorothiazide. Schuirmann's test was highly statistically significant (P<0.001 for perindopril + indapamide versus captopril + hydrochlorothiazide; P<0.002 for perindopril + indapamide versus enalapril + hydrochlorothiazide), so that the two one-sided hypotheses that the treatments were not equivalent were rejected at the nominal level of alpha = 0.05. Similarly, the safety of the treatments was equivalent in terms of serum potassium. The 90% confidence intervals of the differences between perindopril + indapamide and the other treatments were -8.7, -1.6% for captopril + hydrochlorothiazide (P = 0.004) and -1.5, +2.7% for enalapril + hydrochlorothiazide (P<0.001). CONCLUSIONS: We conclude that the safety and efficacy of perindopril + indapamide, captopril + hydrochlorothiazide and enalapril + hydrochlorothiazide were equivalent after 8 weeks of treatment in patients with mild to moderate hypertension.

Adolescent↗
PubMed1996

[Indapamide--a substitute diuretic for hypertensives with hyperglycemia and/or dyslipidemia].

Diuretics are among the first drugs offered to the hypertensive patient. However, they can induce metabolic changes resulting in cardiovascular insult. Especially noteworthy are increased levels of glucose and lipids. Indapamide is a diuretic and vasodilator that does not raise blood glucose or lipid levels. We therefore investigated its use as a substitute diuretic in patients whose treatment had resulted in hyperglycemia and/or hyperlipidemia. In 24 hypertensives, Indapamide, 2.5 mg daily, replaced the diuretic therapy they were receiving. Blood pressure, blood glucose, hemoglobin A1C and lipid profile were measured before and every month during the 6 months of Indapamide treatment. Replacement of diuretics with Indapamide significantly reduced blood glucose from 148 +/- 53 mg/dl to 127 +/- 37, p = 0.05 HbA1C from 8.42 +/- 0.4 mg/dl to 7.7 +/- 2.0, p = 0.05; total cholesterol from 253 +/- 45 mg/dl to 228 +/- 43, p < 0.05; and triglycerides from 224 +/- 145 mg/dl to 176 +/- 91, p < 0.05. Blood pressure was better controlled with Indapamide than with previous medications. It was reduced from an average of 155 +/- 1 systolic and 89 +/- 8 diastolic (mm Hg), to 142 +/- 13 and 83 +/- 7, respectively, p < 0.05. We conclude that Indapamide is safe and effective in lowering blood pressure and contributes to better control of blood glucose and lipid levels in diabetic and dyslipidemic patients, compared to standard diuretics.

Antihypertensive Agents↗
PubMed1996

[Treatment of hypertension with indapamide 1.5 mg sustained-release form: synthesis of results].

In accordance with international recommendations on the need to decrease doses of antihypertensive drugs, a low-dose (1.5 mg) sustained-release form of indapamide was developed so as to optimize the safety/efficacy ratio, while maintaining a once-daily administration. The new formulation ensures that the active ingredient release occurs in a sustained manner over 24 hours, with mean concentrations close to the maximal concentration over a prolonged period, while avoiding peak plasma concentrations. Clinical data were obtained mainly through two European multicenter, randomized, double-blind trials, totalling 690 patients. Firstly, the antihypertensive efficacy' of the new indapamide 1.5 mg form was demonstrated by measuring blood pressure 24 hours after the last drug intake, using a mercury sphygmomanometer; the equivalence of its antihypertensive efficacy with the immediate-release form of indapamide 2.5 mg was then verified. Biochemical safety data showed better acceptability with indapamide 1.5 mg with in particular a reduction of more than 50% of the number of patients with kalemia < 3.4 mmol/l; clinical safety data confirmed the good acceptability observed with the 2.5 mg immediate-release form of indapamide since many years, especially regarding glucose and lipid neutrality. In conclusion, the 1.5 mg sustained-release form of indapamide has an improved antihypertensive efficacy/safety ratio which is in accordance with international recommendations for the usage of low doses of antihypertensive drugs and diuretics in the first-line treatment of hypertension.

Adolescent↗
PubMed1999

Efficacy of indapamide in central diabetes insipidus.

BACKGROUND: Central diabetes insipidus (CDI) results from deficient vasopressin (antidiuretic hormone) secretion and causes polydipsia and polyuria. Desmopressin, a synthetic analog of vasopressin, is the drug of choice in the treatment of CDI, but in mild cases, there are alternative drugs that can be used, including chlorpropamide, carbamazepine, and thiazides. METHODS: In this study, we investigated the efficacy of treatment with indapamide, which is an antihypertensive diuretic oral agent, in 20 consecutive patients with CDI. The diagnosis of CDI was established by water-deprivation and vasopressin tests. Before the study, serum and urinary osmolality, daily urinary volume, and serum electrolyte levels were measured in all 20 patients. Indapamide (2.5 mg/d) was administered for 10 days, and then the investigations were performed again; for purposes of comparison, 250 mg/d of chlorpropamide was also administered to 11 of the 20 patients who had been given indapamide. RESULTS: Indapamide revealed a 40.56% +/- 9.70% (mean +/- SD) (range, 19.6%-55.0%) reduction in 24-hour urinary volume and an increase in urinary osmolality, as well as a decrease in serum osmolality, and was as effective as chlorpropamide (P<.05) in the treatment of CDI. CONCLUSION: Because of its low cost and lack of significant adverse effects, indapamide may be a suitable, easy-to-use alternative oral agent for some patients with CDI.

Adolescent↗
PubMed1995

Efficacious response with lower dose indapamide therapy in the treatment of elderly patients with mild to moderate hypertension.

A low dose (1.25 mg) of indapamide (Lozol, Rhône-Poulenc Rorer Pharmaceuticals, Collegeville, PA) was evaluated in 222 elderly patients (> or = 50 years) with mild to moderate essential hypertension in a multicenter, randomized, double-blind, parallel-group clinical trial. A 4-week single-blind placebo washout period was followed by an 8-week double-blind treatment period. Patients were randomized to receive indapamide 1.25 mg/day or to receive placebo. The primary efficacy variable was the mean change in sitting diastolic blood pressure from baseline to week 8. Eighty-one patients in the indapamide group (73%) and 87 patients in the placebo group (78%) completed the 8 weeks of double-blind therapy. Therapy with 1.25 mg of indapamide produced greater reductions compared with placebo in sitting diastolic blood pressure after 8 weeks of therapy, with statistical significance (P < or = 0.0015) seen after only 2 weeks of therapy and continuing throughout the 8 weeks. All secondary efficacy measures (sitting systolic blood pressure, standing systolic and diastolic blood pressures, and > or = 10 mm Hg decrease or final value of < or = 90 mm Hg in sitting diastolic blood pressure) also showed superior (P < or = 0.0014) improvement in the indapamide group compared with placebo after 8 weeks of double-blind treatment. During the 8-week double-blind treatment period, incidence rates for all adverse events and for drug-related adverse events were similar between the two treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1978

Fluorometric assay for urinary indapamide.

A sensitive fluorescence method for the determination of indapamide was developed. Reaction of indapamide with sodium hydroxide at 100 degrees yielded a fluorescent product, and addition of formaldehyde to the fluorescent product increased its fluorescence intensity by a factor of three. The assay is sensitive to levels of indapamide of 0.025 microgram/ml in an aqueous solution, and a linear response between 0.025 and 2.0 microgram/ml was observed. The procedure was adapted to the analysis of intact indapamide in urine. Concentrations of indapamide of 0.05 microgram/ml can be detected in dogs given 20 mg of the drug.

Animals↗
PubMed1981

Pharmacokinetics of indapamide in dogs.

Four beagle dogs received both an oral and intravenous dose (1 mg/kg) of indapamide in a crossover design. The blood levels and urinary excretion of intact indapamide were measured, and the pharmacokinetic parameters of the drug were defined. The results indicate that indapamide is completely bioavailable after an oral dose and does not undergo first-pass metabolism. Excretion of unchanged drug from the kidney accounted for only a small percentage of the drug's clearance. While the dog is very similar to the human in its handling of indapamide, the dogs clears indapamide approximately twice as fast as humans.

Administration, Oral↗
PubMed1984

Effect of indapamide on renal plasma flow, glomerular filtration rate and arginine vasopressin in plasma in essential hypertension.

Renal plasma flow (RPF), glomerular filtration rate (GFR), arginine vasopressin in plasma (AVP), free water clearance (CH2O) and blood pressure (BP) were determined in 11 patients with essential hypertension at the end of 3 consecutive periods of observation each of 6 of weeks duration; indapamide 2.5 mg daily was given in period 2 and placebo in periods 1 and 3. RPF and GFR were reduced by 9% and BP by 9%/14% supine and 14%/12% standing during indapamide treatment. Changes in renal haemodynamics were not correlated with those in BP. AVP was not significantly altered by indapamide and was not correlated with BP. Indapamide reduced CH2O possibly due to the reduction in GFR. It is concluded that indapamide evidently induces redistribution of the cardiac output, with enhanced muscle blood flow and reduced renal perfusion, and that AVP does not seem to be involved in blood pressure regulation in mild to moderate essential hypertension under basal conditions.

Adult↗
PubMed1990

Clinical efficacy and quality of life with indapamide alone or in combination with beta blockers or angiotensin-converting enzyme inhibitors.

A multicenter study was performed to assess the efficacy and the acceptability of indapamide in hypertensive patients previously untreated, or treated and unsatisfactorily controlled with either angiotensin-converting enzyme (ACE) inhibitor or beta-blocking therapy. Four centers participated in the study, which included patients whose supine diastolic blood pressure was between 95 and 115 mmHg with no treatment (group I, n = 40), those taking captopril (group II, n = 40) or those taking propranolol (group III, n = 40). After a 2-week single-blind placebo run-in period, patients received indapamide either alone (group I) or in combination with the previous therapy (groups II and III) for 4 months. Blood pressure, heart rate, weight, and clinical and biochemical acceptability were measured before and after 2 and 4 months of treatment. At the same time points, quality of life was determined using standardized questionnaires completed by the patient (20 items) and the physician (10 items) and a visual analog scale completed by the patient. In all groups, administration of indapamide induced a clinically and statistically significant reduction in both systolic and diastolic blood pressures in the supine position after 2 months. Indapamide alone controlled blood pressure in 82% of the patients previously untreated, and indapamide in combined therapy controlled blood pressure, respectively, in 67 and 85% of patients previously uncontrolled with ACE inhibitors or beta blockers. In all groups, questionnaires on quality of life showed a progressive and significant improvement in general well-being. After 4 months of treatment, the percentage of improvement in the physician questionnaire was 77.1% in group I, 60.6% in group II and 71.4% in group III.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Identification and pharmacological properties of binding sites for the atypical thiazide diuretic, indapamide.

[3H]Indapamide bound to a single class of binding sites in pig renal cortex membranes with a dissociation constant Kd = 35 +/- 13 nM and a binding site density Bmax = 40 +/- 9 pmol/mg of protein. [3H]Indapamide binding was inhibited by the carbonic anhydrase inhibitor, acetazolamide, and by thiazide diuretics with the following rank order of potency: chlorothiazide greater than hydrochlorothiazide approximately metolazone greater than hydroflumethiazide. The effect of the latter drugs to inhibit [3H]indapamide binding was not related to their activity as thiazide diuretics, but was significantly correlated with their inhibitory effect on carbonic anhydrase II. These results suggest that the major renal binding site of [3H]indapamide is a membrane form of carbonic anhydrase. Inhibition of carbonic anhydrase may play a role in the antihypertensive effect of indapamide.

Animals↗
PubMed1992

Direct vascular actions of hydrochlorothiazide and indapamide in isolated small vessels.

The mechanism by which thiazides lower peripheral resistance is unresolved. The aim of this study was to investigate the mechanisms of the acute vasodilator action of hydrochlorothiazide and the 'thiazide-like' diuretic indapamide on human, guinea pig and rat small arteries. Vessels were mounted on a myograph and the relaxation profile of both drugs and interactions with K+ channels and the vascular eicosanoid system were studied. Neither drug had any relaxant effect in rat mesenteric vessels and indapamide did not relax human arteries. Hydrochlorothiazide in both human and guinea pig vessels produced significantly more relaxation of noradrenaline than K(+)-constricted vessels (P less than 0.001). Relaxation to hydrochlorothiazide was reduced in the presence of charybdotoxin. Maximal-induced hydrochlorothiazide relaxation was reduced by 64% in human arteries (P less than 0.001) and by 91% in guinea pig vessels (P less than 0.001). Incubation with glibenclamide and indomethacin had no effect on the relaxant activity of hydrochlorothiazide and indapamide. Indapamide-induced relaxation was unaffected in the presence of charybdotoxin. These results show marked differences in the acute vasodilator action of hydrochlorothiazide and indapamide. There appears to be involvement of Ca(2+)-activated K+ channels in the acute vasorelaxant activity of hydrochlorothiazide.

Animals↗
PubMed1996

Indapamide regresses, but transdermal clonidine does not regress, left ventricular hypertrophy in hypertensive diabetic patients.

This report describes the effects of indapamide versus transdermal clonidine on left ventricular hypertrophy (LVH) in hypertensive diabetic patients. A sample of 24 hypertensive diabetic men, aged 40-68 years, with echocardiographically proven LVH was equally divided in to 2 groups. Group 1 was treated with indapamide 2.5 mg/day, and group C with transdermal clonidine weekly. Left ventricular mass and posterior wall and septal thickness were measured by standard echocardiograms done at baseline and every 6 months. At 24 months, treatment crossover was done. Normotension was maintained throughout the study. With indapamide, LVH regression was measurable at 6 months, and left ventricular mass had returned to normal after 18 months. Transdermal clonidine did not regress LVH, but when the patients were switched to indapamide, LVH did regress. Clonidine maintained normal ventricular dimensions after regression had been induced by indapamide.

Administration, Cutaneous↗