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PubMed1988

Antihypertensive therapy in diabetic patients. The use of indapamide.

Abnormalities in glucose tolerance in nondiabetic patients and rapid alteration in non-insulin-dependent diabetics have been reported with antihypertensive drugs such as beta-blockers or thiazide diuretics. Such deleterious effects on a cardiovascular risk factor could limit the long-term benefit of an antihypertensive treatment. Indapamide is a nonthiazide antihypertensive agent that appears to respect the glucose tolerance in hypertensive patients. The present study was conducted to assess the effects of indapamide 2.5 mg in 10 hypertensive non-insulin-dependent diabetic patients treated for a one-year period. Glucose tolerance was evaluated using a 50-g oral glucose test, with measurements of plasma glucose and insulin before and after treatment. At the end of the one-year treatment, both systolic and diastolic blood pressure were significantly reduced, whereas there was no significant alteration in either plasma glucose or plasma insulin levels. Thus, indapamide appears as an effective antihypertensive agent in the diabetic patient, with no adverse effects on the glucose tolerance.

Blood Glucose↗
PubMed1988

Comparative study on the antihypertensive efficacy of torasemide and indapamide in patients with essential hypertension.

In a double-blind randomized multicenter study the antihypertensive efficacy of 2.5 mg torasemide (1- isopropyl-3-([4-(3-methyl-phenylamino)pyridine]-3-sulfony)urea) and 2.5 mg indapamide was compared in patients with essential hypertension, known as responders to diuretic therapy. After a wash-out period of 4 weeks patients with a sitting diastolic blood pressure of 100-115 mmHg were included in the 12-weeks active treatment period. After 4 weeks of treatment with a once daily 2.5 mg dose of each drug, doses could once be doubled if blood-pressure decrease was considered to be insufficient. 66 patients qualified for the statistical evaluation, 32 in the torasemide group and 34 in the indapamide group. In these patients both drugs caused a similar fall in blood pressure leading to a normalization of blood pressure in most of the patients. Serum parameters remained within normal limits. Only serum potassium was significantly lower with 2.5 mg indapamide compared to 2.5 mg torasemide at the end of the study. No side effects were reported for both drugs. As the lowest effective dose of a diuretic should be used for the treatment of hypertensive patients, 2.5 mg torasemide, which is below the threshold dose for significantly enhanced diuresis, seems to be the recommended dose for antihypertensive treatment.

Adult↗
PubMed1988

Effect of indapamide on an experimental model of cerebral ischemia in hypertensive rats.

This study quantified the immediate general hemodynamic events following the bilateral carotid ligation-induced cerebral ischemia in normotensive and spontaneously hypertensive rats. The influence of treatment with indapamide was evaluated. In normotensive rats, hemodynamic values remained unchanged during the 10 minutes following the carotid ligation. In spontaneously hypertensive rats, arterial pressure values immediately and significantly (p less than 0.01) increased, up to 50 percent during the 10 minutes following the carotid ligation. Heart rate was unchanged. Indapamide at a short-term 3 mg/kg intraperitoneally, chosen in order to give a minimal (nonsignificant) antihypertensive effect in spontaneously hypertensive rats, significantly (p less than 0.01) reduced the bilateral carotid ligation-induced vasopressor response, whereas heart rate remained unchanged. The results presented here show that in spontaneously hypertensive rats, but not in normotensive rats, bilateral common carotid ligation induces an immediate and strong increase in arterial pressure values. These results compare with the previously described differences in cerebral ischemia-induced disorders in normotensive and hypertensive rats. Finally, indapamide, an antihypertensive agent that decreases vascular reactivity, significantly inhibits the carotid ligation-induced vasopressive response in hypertensive rats.

Animals↗
PubMed1985

Clinical evaluation of muzolimine and indapamide during treatment for essential hypertension.

Muzolimine, a new saliuretic, has been shown to combine high ceiling and long-acting effects in animal experiments. This study was designed to examine whether this desirable combination of effects, which up until the present time has not been incorporated into any substance also occurs during patient treatment. Fifty-three patients with mild essential hypertension (WHO groups I and II) in three medical centers were treated with either muzolimine or indapamide, which served as the reference preparation, in a randomised, double-blind study. After a two week run-in phase during which the patients received placebo, half of the patients received 20 mg muzolimine and the other half 2.5 mg indapamide once daily. Eight weeks of therapy were followed by a 2 week follow-up phase, during which placebo was dispensed. During the trial period a weekly clinical examination was performed including the measurement of blood pressure, pulse, hematocrit, electrolytes, uric acid, glucose, creatinine and lipid status. An electrocardiogram and Schellongtest were conducted every two weeks. Patients were instructed to keep a diary in which they were to note drug related complaints. Statistical analysis was carried out using the Pratt-Wilcoxon Pair Test. Differences were judged significant at the 5% level. Both muzolimine and indapamide were tolerated well with minimal side effects, which however, did not make it necessary to discontinue treatment. Both preparations induced mild blood pressure reductions of approximately 10 and 5 mmHg for the systolic and diastolic blood pressure, respectively. Two weeks after cessation of muzolimine treatment neither systolic nor diastolic blood pressure showed any significant difference to values achieved during the treatment phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Haemodynamic changes in peripheral arterial circulation during antihypertensive treatment with captopril, methyldopa and indapamide.

Structural changes in resistance vessels of the lower limbs have been detected in early stages of arterial hypertension. In these patients it might be important to reduce blood pressure by drugs which do not impair peripheral blood flow. Twenty-four patients with arterial hypertension, without target organ damage were randomly given a placebo, 50 mg captopril, 500 mg methyldopa or 2.5 mg indapamide and their blood pressure, arterial blood flow and peripheral resistance were measured at baseline and at the peak action of the antihypertensive treatment. Significant decreases in blood pressure and peripheral resistance have been induced by a single oral dose of captopril and methyldopa: a concomitant significant increase in peripheral blood flow to the lower limbs was also observed during methyldopa treatment. No acute effect was observed on the placebo or on indapamide: the latter induced a decrease in blood pressure and in peripheral resistance along with an increase in arterial blood flow during long-term treatment after four weeks of therapy. Our observations seem to support the usefulness in hypertensive patients with concomitant lesions in the peripheral arterial tree of antihypertensive agents such as methyldopa and indapamide which increase blood flow and reduce peripheral resistance while lowering high blood pressure.

Adult↗
PubMed1984

The efficacy of indapamide in hypertensive patients failing to respond to a beta-blocker alone.

A double-blind, placebo-controlled, cross-over study was carried out to evaluate the efficacy and safety of 2.5 mg indapamide in 24 hypertensive patients failing to respond to oxprenolol alone. An additional 6 patients were assessed by ambulatory blood pressure recordings over a 15-hour period with a Remler M2,000 semi-automatic sphygmomanometer. On average, indapamide reduced supine blood pressure by 18.5/10 mmHg and standing blood pressure by 19.6/8.9 mmHg. The ambulatory recordings carried out in 6 patients detected a fall in diastolic pressure not observed using clinic readings in these 6 patients, suggesting that this is a more sensitive method of detecting antihypertensive effect. These responses were not associated with significant changes in heart rate or body weight and there was no significant postural fall in blood pressure. No serious side-effects were reported. Changes in serum potassium, chloride and urate similar to those seen with diuretics were observed. These results suggest that indapamide is a useful and safe adjunct to beta-adrenoceptor blocking therapy for uncontrolled hypertension.

Adult↗
PubMed1983

Urinary magnesium output after a single dose of indapamide in healthy adults.

Twenty-four hour urinary volume and output of chloride, sodium, potassium, calcium, magnesium, phosphate, zinc, creatinine and urea were measured under strictly controlled experimental conditions in 7 biologically comparable healthy volunteers given separate single doses of placebo and indapamide 2,5 mg. Indapamide significantly increased the urinary volume and the output of Cl-, Na+, K+ and urea but reduced output of Ca2+ and creatinine. Since Mg2+ output over 24 hours was unaffected, the prolonged use of indapamide at the dose studied may not promote the occurrence of cardiac arrhythmias and sudden death in spite of the significant K+ losses measured.

Adolescent↗
PubMed1981

The pharmacology and clinical pharmacology of indapamide.

At low doses indapamide is a potent and long acting antihypertensive agent in various hypertensive animals and in man, but is without activity in normotensive subjects. A daily dose of 2.5 mg produces a minimal diuresis but at higher doses this increases without any significant augmentation of hypotensive activity. It appears to have no effect on most blood biochemical parameters, including glucose, high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglycerides, noradrenaline, adrenaline, but potassium levels may decrease and uric acid and renin increase. Indapamide had no effect on renal function nor does it alter left ventricular function, electrocardiograph (ECG) or heart rate, although cardiac output may marginally increase. Total peripheral resistance is significantly decreased and it may exert its antihypertensive effect by reducing vascular reactivity to various pressor stimuli by inhibiting the net inward flow of calcium and resultant phasic contractions in vascular smooth muscle. Indapamide differs from the diuretics in that it has a comparatively high lipid solubility; it is also bound to blood proteins and elastin in vascular smooth muscle and little is eliminated in the urine. It may be for these reasons that the drug has less diuretic activity but more pronounced effect on vascular smooth muscle than compounds of similar structure.

Animals↗
PubMed1981

The effect of indapamide on muscle blood flow in hypertensive patients.

The effect of indapamide on the peripheral circulation was investigated in hypertensive patients using a xenon washout technique. Resting muscle blood flow increased by 38% after 1 week's treatment in 5 patients and by 52.6% after 6 weeks treatment in 4 patients. Exercise muscle blood flow increased by 18% in 4 patients after 6 weeks' treatment. Resting supine and standing blood pressure was decreased by indapamide after 2, 4 and 6 weeks of treatment. Exercise systolic blood pressure was not changed by indapamide. The results in this pilot study suggest that peripheral resistance is reduced by a direct action on the vessel wall.

Antihypertensive Agents↗
PubMed1981

Indapamide in ambulant treatment of hypertension: a comparative study with alpha-methyldopa.

Indapamide and methyldopa were compared in an open parallel study in patients with mild or moderate hypertension. Both drugs showed an antihypertensive effect significantly different from placebo but with indapamide the blood pressure response occurred sooner, after 2 weeks, as opposed to 4 weeks with methyldopa. Indapamide was better tolerated than methyldopa, producing fewer side effects.

Antihypertensive Agents↗
PubMed1993

Regression of microalbuminuria: results of a controlled study, indapamide versus captopril.

Our aim was to assess the effect of blood pressure treatment on albumin excretion rate (AER) in diabetic patients using two antihypertensive agents with different modes of action: indapamide and captopril. Patients with persistent microalbuminuria on two occasions (AER 20-200 micrograms/min) entered a randomized crossover study of 12 weeks of therapy with a constant dose of either indapamide 2.5 mg daily or captopril 12.5 mg three times daily, with a 4-week washout between therapy periods. Blood pressure was measured using a random-zero sphygmomanometer and AER by radioimmunoassay on a timed urine collection. Results (mean +/- standard deviation) were analyzed by repeated measures of analysis of variance after log transformation of AER data. Twelve patients [nine men; mean age 58 +/- 7.5 years (range 49-73 years), all with non-insulin-dependent diabetes mellitus (NIDDM)] were studied. Both blood pressure [initial mean systolic 144 +/- 14 mm Hg (range 124-166)/initial mean diastolic 85 +/- 6 mm Hg (range 75-96)] and AER [initial 92 +/- 36 micrograms/min (range 36-161)] were significantly reduced below basal levels (at the 0.05 level) at all study intervals by both antihypertensive agents. The results show the importance of blood pressure and its treatment on AER in patients with NIDDM. In this study, indapamide was as effective as an angiotensin-converting enzyme inhibitor in reducing both blood pressure and microalbuminuria.

Aged↗
PubMed1993

[The effect of indapamide on phosphate metabolism in hypertensive patients].

Twenty-four patients were studied to assess the efficacy and principle of indapamide in hypertensive patients previously treated and unsatisfactorily controlled with either angiotensin-converting enzyme (ACE) inhibitor or atenolol therapy. The result showed a satisfactory anti-hypertensive effect of indapamide. Plasma phosphate concentrations were markedly reduced and no significant variance in plasma K+, Na+ and Ca+ concentration after two weeks of indapamide therapy (2.5 mg, one day). Thus indapamideinduced reduction of blood pressure could be mediated by an effect of this drug on phosphate balance.

Adult↗
PubMed1993

[The influence of indapamide on 6-keto-PGF1 alpha, PGE2, and PGF2 alpha synthesis and plasma TXB2 levels in spontaneously hypertensive rats].

The influence of indapamide on the prostaglandin system was studied in spontaneously hypertensive rats (SHR) and compared with SHR control and normal WKY rats. The results show that the synthesis of vasoconstrictive prostaglandins (PGE2 and PGF2 alpha) in the renal medullary tissues of SHR is higher than that of normal rats, and this may have something to do with the development and maintenance of high blood pressure in SHR. After indapamide administration, the synthesis of prostacyclin in SHR aorta increased significantly as compared with the SHR control group, whereas PGE2 and PGF2 alpha production in renal medullary tissues decreased markedly. The results support the idea that the prostaglandin system, especially PGE2 and PGF2 alpha, plays an important role in the antihypertensive mechanism of indapamide.

6-Ketoprostaglandin F1 alpha↗
PubMed2003

Effects of blood pressure lowering with perindopril and indapamide therapy on dementia and cognitive decline in patients with cerebrovascular disease.

BACKGROUND: High blood pressure and stroke are associated with increased risks of dementia and cognitive impairment. This study aimed to determine whether blood pressure lowering would reduce the risks of dementia and cognitive decline among individuals with cerebrovascular disease. METHODS: The Perindopril Protection Against Recurrent Stroke Study (PROGRESS) was a randomized, double-blind, placebo-controlled trial conducted among 6105 people with prior stroke or transient ischemic attack. Participants were assigned to either active treatment (perindopril for all participants and indapamide for those with neither an indication for nor a contraindication to a diuretic) or matching placebo(s). The primary outcomes for these analyses were dementia (using DSM-IV criteria) and cognitive decline (a decline of 3 or more points in the Mini-Mental State Examination score). RESULTS: During a mean follow-up of 3.9 years, dementia was documented in 193 (6.3%) of the 3051 randomized participants in the actively treated group and 217 (7.1%) of the 3054 randomized participants in the placebo group (relative risk reduction, 12% [95% confidence interval, -8% to 28%]; P =.2). Cognitive decline occurred in 9.1% of the actively treated group and 11.0% of the placebo group (risk reduction, 19% [95% confidence interval, 4% to 32%]; P =.01). The risks of the composite outcomes of dementia with recurrent stroke and of cognitive decline with recurrent stroke were reduced by 34% (95% confidence interval, 3% to 55%) (P =.03) and 45% (95% confidence interval, 21% to 61%) (P<.001), respectively, with no clear effect on either dementia or cognitive decline in the absence of recurrent stroke. CONCLUSIONS: Active treatment was associated with reduced risks of dementia and cognitive decline associated with recurrent stroke. These findings further support the recommendation that blood pressure lowering with perindopril and indapamide therapy be considered for all patients with cerebrovascular disease.

Aged↗
PubMed1991

A double-blind, randomized, placebo-controlled comparison of the metabolic effects of low-dose hydrochlorothiazide and indapamide.

To compare the metabolic effects of indapamide (I) and hydrochlorothiazide (HCTZ) at equivalent hypotensive doses, 11 hypertensive patients (5 male, 8 black, aged 56 +/- 8 yr--mean +/- SEM) having serum uric acid concentrations greater than 8.0 mg/dL while receiving previous therapy with thiazides, received 28-day courses of placebo, indapamide (2.5 mg/d), and HCTZ (25 mg/d) in randomized, double-blind, double-crossover design. Supine and standing blood pressures, weight, pulse rates and sera were obtained after each 28 day period. Blood pressures and weights were lowered (P less than .001 and 0.01, respectively) equally by the diuretics: supine blood pressures fell from 168 +/- 4/104 +/- 2 (placebo) to 153 +/- 4/93 +/- 2 (HCTZ) and 155 +/- 4/94 +/- 2 mm Hg (I); standing blood pressures (after 2 minutes upright) also decreased: 171 +/- 5/104 +/- 2 (placebo) to 156 +/- 5/93 +/- 2 (HCTZ) and 157 +/- 4/94 +/- 2 mm Hg (I). There was a statistically significant difference (P less than .05) across treatments by analysis of variance in both uric acid and potassium concentrations: serum urate (in mg/dL) was lowest with placebo (7.1 +/- 0.3), and rose to 8.3 +/- 0.2 with HCTZ (P less than .001 compared with placebo by paired t test), and 8.1 +/- 0.2 with I (P less than .005 vs. placebo). The urate concentration with I was significantly lower than that with HCTZ (P less than .02), but the magnitude of the difference was small (0.2 mg/dL).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1982

Pharmacokinetics and bioavailability of indapamide--a new antihypertensive drug.

Two formulations of indapamide tablets (2.5 mg) were given as a 5.0 mg dose and the subsequent blood levels were compared to those obtained after administration of a 5.0 mg solution. The study was conducted as a randomized three-way crossover design using healthy male volunteers. The drug was well tolerated by all the subjects involved. The area under the blood concentration versus time curve, extrapolated to infinity was essentially the same for all three formulations (4.2, 4.7, and 4.4 microgram-h/ml). Statistical comparison of the blood levels from the two tablets showed that one tablet had a significantly shorter time of maximum blood concentration (2.3 vs 3.5). Cmax(333ng/ml) and tmax (0.7h) values for the solution were significantly higher than either tablet. The average half-life (beta-phase) for all three formulations was 15 h, while the average systemic clearance was 20 ml/min. Indapamide has a low clearance rate and there was no evidence that the drug undergoes a first-pass effect.

Adolescent↗
PubMed1985

Nadolol in combination with indapamide and xipamide in resistant hypertensives.

Twenty-four hypertensive patients have been studied. All had blood pressure recordings greater than 160/95 mmHg on 3 occasions whilst taking a beta blocker and two other antihypertensive agents in therapeutic doses. Compliance was checked by intermittent urine analysis for the relevant beta-blocker. These difficult to control hypertensives were treated with nadolol alone, nadolol plus indapamide and nadolol plus xipamide each for 2 months in random order. The aim was to reduce the blood pressure to below 160/95 mmHg. The supine blood pressure on nadolol alone (167/100 mmHg) was comparable to that on the previous three drug regimens (157/100 mmHg), the other two treatments were more effective (145/90 and 148/93 mmHg respectively). Hypokalaemia (serum potassium below 3.5 mmol/l) occurred in six individuals but occurred more frequently on xipamide than on indapamide.

Adult↗
PubMed1981

Diuretic treatment and serum lipoproteins: effects of tienilic acid and indapamide.

Treatment with the commonly used diuretic, chlorthalidone, has previously been found to increase the serum low-density-lipoprotein cholesterol (LDL-C) fraction. Therefore, the effects of two new agents, tienilic acid (a combined diuretic-uricosuric) and indapamide on serum lipid and lipoprotein levels were assessed. Six weeks of treatment with tienilic acid, 250 mg/day, markedly decreased serum uric acid and significantly increased LDL-C and triglycerides in 16 men. In contrast, indapamide 2.5 mg/day, had no apparent influence on serum lipids or lipoproteins in 18 men.

Diuretics↗