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PubMed1996

Inhibition of human thiopurine methyltransferase by furosemide, bendroflumethiazide and trichlormethiazide.

RESULTS: Incubation in vitro of human recombinant and erythrocyte (RBC) thiopurine methyl transferase (TPMT) with furosemide, bendroflumethiazide and trichlormethiazide demonstrated inhibition of both enzyme preparations, with IC50 values of 170 microM, 360 microM and 1 mM, respectively. Kinetic studies revealed that the inhibition was mixed or non-competitive with regard both to the thiopurine substrate 6-mercaptopurine (6-MP) and the methyl donor S-adenosyl-L-methionine. CONCLUSION: Since S-methylation is a major pathway in the metabolism of thiopurines, our data point to the possibility of a clinically significant diuretic-thiopurine interaction in patients treated simultaneously with these drugs.

Bendroflumethiazide↗

PubMed1998

Determination of trichlormethiazide in bovine milk by high-performance liquid chromatography.

A liquid chromatographic procedure was developed and validated for the quantitative determination of trichlormethiazide (TCMTZ) in bovine milk. Whole milk was defatted by initial centrifugation at 4 degrees C. The resulting skim milk was treated with lead acetate and acetonitrile, vortex mixed, and centrifuged. The acetonitrile from the supernatant was back extracted in ethyl acetate. The organic solvent mixture which contained TCMTZ was further treated with sodium tungstate, vortex mixed, and centrifuged. The top organic layer was removed and evaporated to dryness; the resulting residue was reconstituted in the mobile phase, and the final extract was analyzed by high-performance liquid chromatography (HPLC). The HPLC conditions employed included a polymer column, a mobile phase consisting of 30% acetonitrile or 30% acetonitrile-tetrahydrofuran (2:1, v/v) in a phosphate buffer (pH 3), and a UV detection at 225 nm. The average recoveries of TCMTZ from milk fortified at 7, 14, 35, 70, and 140 ppb were 88, 93, 117, 110, and 99%, respectively, with corresponding C.V. values of 7, 18, 11, 9, and 21%. The method was validated by assaying milk obtained from a cow dosed with Naquasone. TCMTZ concentration was detected only in the 8 h post dose milk samples and was determined to be 6 ppb.

Animals↗

PubMed1985

[A trichlormethiazide-amiloride combination in essential hypertension].

Following a placebo period of 2 weeks 39 patients with essential hypertension were given during 4 weeks a combination of 2 mg trichlormethiazide and 2 mg amiloride (Esmalorid). If the blood pressure was adequately reduced treatment was continued for a further 4 weeks; if not, a double dose was dispensed during the second 4-week period. Patients with a diastolic blood pressure under 90 mm Hg after 8 weeks when treated with a 1 mg dose, were subsequently treated with a 1 mg dose for a period of 3 months. After 8 weeks of treatment mean systolic blood pressure was reduced from 167 +/- 17 mm Hg to 151 +/- 19 mm Hg (sitting) and from 163 +/- 15 mm Hg to 148 +/- 18 mm Hg (standing), while mean diastolic blood pressure was decreased from 104 +/- 6 mm Hg to 93 +/- 8 mm Hg (sitting) and from 105 +/- 6 mm Hg to 94 +/- 8 mm Hg (standing). In 29 patients diastolic blood pressure had dropped to values under 95 mm Hg. Serum potassium remained constant during the treatment except for three patients with values outside the normal range (3.3, 3.4 and 5.2 mmol/l). The other serum electrolytes, glucose, creatinine, blood lipids, transaminases, hemogram, as well as body weight and heart rate remained unchanged. Two patients complained of side effects and did not complete the study. All other patients tolerated the treatment well.

Adult↗

PubMed2000

New oral dosage form for elderly patients. III. Stability of trichlormethiazide in silk fibroin gel and various sugar solutions.

The hydrolysis of trichlormethiazide (TCM) in silk fibroin gel (SFG) prepared in various sugar solutions (such as ribose, fructose, mannose, and glucose solutions) was determined. The hydrolysis rate of TCM differed with the variety of sugars utilized in this study; that is, it decreased in the following order: ribose > fructose > mannose > glucose. To investigate the relationship between the hydrolysis rate of TCM and the physicochemical properties of the sugar molecule, the amount of unfrozen water of sugar molecules was calculated from differential scanning calorimetry (DSC). The amount of unfrozen water increased with an increase in the number of the equatorial OH groups n(e-OH) per sugar molecule that are able to hydrate favorably to the surrounding water molecules. The hydrolysis rate constant decreased with increase in n(e-OH); glucose, having a large n(e-OH) in this study could effectively stabilize TCM.

Administration, Oral↗

PubMed1988

Site and mechanism of action of trichlormethiazide in rabbit distal nephron segments perfused in vitro.

To determine the exact site and mechanism of action of thiazide diuretics, effects of 10(-4) M trichlormethiazide (TCM) on NaCl transport were examined in the distal convoluted tubule (DCT), the connecting tubule (CNT) and the cortical collecting duct (CCD) of rabbit kidney by the in vitro microperfusion technique. TCM added to the lumen decreased lumen-to-bath 36Cl flux (JCl(LB)) only in the CNT without changing the transmural voltage (VT). In the DCT, 10(-4) M furosemide did not change JCl(LB) even if it was added to the lumen with 10(-4) M TCM, whereas 10(-5) M amiloride in the lumen decreased the lumen-to-bath 22Na flux (JNa(LB)) and VT. In the CNT, TCM added to the lumen did not affect the bath-to-lumen 36Cl flux. Addition of TCM to the bath slightly decreased JCl(LB). Luminal addition of 10(-4) M TCM also decreased JNa(LB). Amiloride at 10(-5) M in the lumen decreased both JNa(LB) and VT. Addition of TCM with 10(-5) M amiloride further decreased JNa(LB) without affecting VT, indicating that TCM affects the electroneutral Na+ transport, which is distinct from the amiloride-sensitive conductive Na+ pathway. When Na+ was removed from the lumen, JCl(LB) was markedly decreased, but addition of TCM did not cause further decrease in JCl(LB). Furosemide did not affect JCl(LB), but addition of both 10(-4) M TCM and furosemide decreased JCl(LB), indicating that Na+-K+-2Cl- cotransport is not involved in the action of TCM. Removal of HCO3- slightly decreased JCl(LB), and TCM caused further decrease in JCl(LB). Amiloride at 10(-3) M, a concentration supposed to inhibit the Na+/H+ antiport, slightly decreased JCl(LB), and addition of TCM caused a further marked decrease in JJl(LB). The similar results were also obtained when the combined effects of 10(-3) M 4,4'-diisothiocyano-stilben-2,2'-disulfonate(DIDS) and 10(-4) M TCM were examined. These findings suggest that the parallel antiport of Na+/H+ and Cl-/HCO3- is not involved in the action of TCM. By excluding other possible mechanisms involving neutral Na+-dependent Cl- transport, we conclude that TCM inhibits Na+-Cl- cotransport in the luminal membrane of the rabbit CNT.

Animals↗

PubMed1978

Antihypertensive effect of trichlormethiazide in spontaneously hypertensive rats.

Antihypertensive and diuretic effects of trichlormethiazide (TCM) were investigated in the spontaneously hypertensive rats (SHR). The antihypertensive effect of TCM in an acute experiment was observed in male SHR only at a dose over 10 mg/kg given intraperitoneally and not in female SHR and normotensive Kyoto Wistar rats. In a subacute experiment (6 weeks), TCM retarded the development of hypertension in the male SHR loaded with 1% saline solution at an oral dose over 1 mg kg-1 day-1 and such had a diuretic effect. Oral administration of TCM and hydrochlorothiazide (HCT) at 10 mg kg-1 day-1 retarded the development of hypertension in the saline loaded female SHR to the same degree, but the relationship between antihypertensive and diuretic effects of both compounds was obscure. Except for decreases of water contents in the thoracic artery and wet weights of hearts, the electrolyte, uric acid, catecholamine and 5-hydroxytryptamine contents in the serum or/and organs were not affected by either TCM or HCT. It is concluded that the antihypertensive effect of TCM and HCT can be observed in SHR with a saline-load, and that the effect may be due to diuretic actions in the male. The relationship was not apparent in female SHR.

Animals↗

PubMed2003

A case of exercise-induced acute renal failure in a patient with idiopathic renal hypouricemia developed during antihypertensive therapy with losartan and trichlormethiazide.

Exercise-induced acute renal failure (ARF) developed in a 45-year-old man during antihypertensive therapy with losartan and trichlormethiazide. The antihypertensive therapy was stopped and marked hypouricemia became apparent during improvement of his renal function. The daily urinary excretion of uric acid was normal and an increased fractional excretion of uric acid was observed. Renal biopsy revealed that the kidney was recovering from acute tubular necrosis with interstitial fibrosis. Based on the results of pyrazinamide and benzbromarone tests, we classified this case as one of presecretory reabsorption defect of uric acid. Antihypertesive therapy with benidipine and candesartan was initiated, and the patient has not had any ARF episodes since. Because idiopathic renal hypouricemia can be associated with exercise-induced ARF and chronic renal dysfunction, careful antihypertensive therapy and follow-up evaluation of renal function might be necessary for hypertensive patients with idiopathic renal hypouricemia.

Acute Kidney Injury↗

PubMed1978

Inhibition by trichlormethiazide of catecholamine release from perfused bovine adrenals.

Effect of thiazides on catecholamine release was examined using perfused bovine adrenal glands in vitro. Thiazides, such as trichlormethiazide and methyclothiazide inhibited catecholamine release evoked by carbamylcholine although they did not inhibit catecholamine release evoked by excess potassium. Thus it seems that these drugs inhibit catecholamine release release by an anticholinergic mechanism. Such inhibitory effect of thiazide on catecholamine release may be involved in the antihypertensive effect of these drugs.

Adrenal Glands↗

PubMed1963