SEARCH · PubMed Health

Results for “METHYCLOTHIAZIDE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources

PubMedDate not supplied

[Home blood pressure monitoring in addition to office blood pressure determination is useful in patients with systolic hypertension before their inclusion into a drug trial].

OBJECTIVE: In patients with uncontrolled systolic hypertension, to estimate the value of home blood pressure monitoring in addition to office blood pressure for inclusion in a trial. METHODS: 80 patients with systolic hypertension, defined as SBP > or =140 mmHg and pulse pressure > or =60 mmHg, were treated for 4 weeks with a thiazide diuretic at usual dose (25 mg HCTZ or 1.5 mg indapamide or methyclothiazide 5 mg). Blood pressure was measured using an automatic monitor (Omron M6) at office and at home in the 3 days prior the visit. Subjects with an uncontrolled hypertension were included in the second part of the trial only if there fulfilled inclusion criteria: office SBP > or =140 mmHg and home SBP > or =135 mmHg (mean of 18 measurements obtained on 3 consecutive days) and office pulse pressure > or =60 mmHg. RESULTS: After 4 weeks with diuretic treatment, 62% of patients fulfilled 3 criteria and were included in the second part of the trial. It was observed 76% of patients with office SBP > or =140 mmHg, 72% with office pulse pressure > or =60 mmHg and 70% with both office SBP and PP criteria. However, only 67% of patients had home SBP > or =135 mmHg. Discrepancy between office and home SBP was observed and subjects with a white coat hypertension was noticed in 14% and masked hypertension in 5%. CONCLUSION: If patients with systolic hypertension have to be included into a drug trial because there are uncontrolled, home blood pressure monitoring in addition to office blood pressure is a very useful criteria for inclusion because misclassifications due to white coat or masked hypertension is frequent in these patients.

Aged↗

PubMed2002

Gas-phase behaviour of negative ions produced from thiazidic diuretics under electrospray conditions.

A systematic mass spectrometric study of 10 thiazidic diuretics and related compounds was undertaken by mass spectrometry (MS) with electrospray ionization in the negative ion mode. Collisional dissociation 'in-source' (CID-MS) and in a low-pressure collision cell (CID-MS/MS) were compared in both excitation regions. Spectra obtained by CID-MS and by CID-MS/MS were matched. Using the two methods, loss of HCl and consecutive dissociations from 2HCl losses were exhibited from compounds such as methyclothiazide and trichlormethiazide but not from other thiazidic diuretics that contain chlorine substituents in the aromatic moiety. However, deprotonated dichlorphenamide gave rise to loss of HCl by CID-MS and CID-MS/MS. For other diuretics such as hydroflumethiazide and hydrochlorothiazide, the loss of HCN and [HCN + SO(2)] was relevant. Reaction mechanisms were checked by means of deuterium-hydrogen exchange, which showed that deprotonation took place regioselectively on the heterocyclic moiety. The cleavage pathways require molecular isomerization forming ion-dipole complexes prior to decompositions, allowing long-distance proton transfer for neutral elimination. Identifications of the most specific fragmentations presented in this paper were applied to the screening and unambiguous identification of diuretics for horse doping control.

Benzothiadiazines↗

PubMed1981

Semiaqueous potentiometric determinations of apparent pKa1 values for benzothiadiazines and detection of decomposition during solubility variation with pH studies.

Apparent acidity constants obtained for various benzothiadiazine diuretics by semiaqueous potentiometric titrations gave satisfactory agreement with many values obtained by aqueous potentiometry. One suitable method for determining the acidity constants of sparingly soluble drugs, the solubility variation with pH technique, does not take into account instability problems. The preparation of decomposition products and the TLC analysis of sample solutions at various time intervals during solubility studies of methyclothiazide and bendroflumethiazide indicated that decomposition takes place during agitation and equilibration. This decomposition in buffers of pH 8 and higher was confirmed with the acidified p-dimethylaminobenzaldehyde test for primary aromatic amines.

Benzothiadiazines↗

PubMedDate not supplied

Effects of riboflavin analogues and diuretics on the spontaneously hypertensive rat heart.

The chronic treatment of spontaneously hypertensive rats (SHR) with 7,8-dimethyl-10-(3-chlorobenzyl) isoalloxazine [CBI], 7,8-diethyl-10-aminol isoalloxazine [DEAI], enduron (methyclothiazide) and amiloride were studied for their effects on blood pressure and cardiac contractile protein ATPase activities. After 35 weeks of treatment all the above antihypertensive agents showed a decrease in blood pressure in the SHR (p less than 0.01). Chronic treatment with CBI, DEAI, enduron, and amiloride significantly improved the myofibrillar ATPase activity at all pCa2+ concentrations (p less than 0.01). Furthermore, CBI, DEAI, enduron, and amiloride drug treatments enhanced actin-activated myosin ATPase activity (p less than 0.01). The Ca2(+)-activated myosin ATPase activity was significantly elevated after treating with CBI and DEAI (p less than 0.01). These results suggest that the antihypertensive agents used in this study helped in reducing the blood pressure with a subsequent increase in myocardial contractile protein ATPase activity.

Actins↗

PubMed1991

Combination antihypertensive therapy with terazosin and other antihypertensive agents: results of clinical trials.

Clinical trials in which the selective alpha 1-adrenergic receptor blocker terazosin was given in combination with other antihypertensive agents are reviewed. Results of a recent study examining the effects of combination terazosin and verapamil therapy on blood pressure and heart rate are also presented. In several studies of the combination of terazosin plus a diuretic (hydrochlorothiazide, methyclothiazide, chlorthalidone, furosemide, amiloride, triamterene, metolazone, or spironolactone), significant decreases in one or more of the blood pressure variables studied were demonstrated (compared with diuretic plus placebo). In a placebo-controlled, double-blind study of terazosin plus atenolol, supine and standing blood pressures decreased significantly from baseline (atenolol monotherapy) after the addition of terazosin but not placebo. In a study of terazosin added to background therapy (including beta-blockers, diuretics, methyldopa, clonidine, captopril, guanethidine, hydralazine, and nifedipine), the addition of terazosin resulted in significant decreases in supine and standing diastolic blood pressures compared with baseline values (background therapy alone). Combination antihypertensive therapy with terazosin and verapamil reduced blood pressure to a significantly greater extent than either agent alone. Preliminary pharmacokinetic results indicate that terazosin did not alter the metabolism of verapamil. No significant abnormal laboratory test results have been reported for patients taking terazosin in combination with other antihypertensive agents; in fact some evidence suggests that terazosin may attenuate adverse lipid, glucose, and potassium changes associated with thiazide diuretics. Adverse experiences associated with terazosin combination therapy are usually mild to moderate. Results from all these studies suggest that terazosin effectively controls mild-to-moderate hypertension when it is used in combination with other antihypertensive agents without cumulative adverse effects.

Adrenergic alpha-Antagonists↗

PubMed1988

UV-A induced DNA nicking activities of skin photosensitive drugs: phenothiazines, benzothiadiazines and afloqualone.

Plasmid pBR 322 was subjected to UV-A irradiation in the presence of photosensitive drugs, i.e., phenothiazines [chlorpromazine hydrochloride (CPZ), promethazine hydrochloride (PMZ) and mequitazine (MQZ)], benzothiadiazines [penflutizide (PFZ), hydrochlorothiazide (HCT) and methyclothiazide (MCT)] and afloqualone (AQ). The distribution of the closed-circular and the open-circular form of the plasmid DNA was analyzed by means of neutral agarose gel electrophoresis. All the drugs used induced more or less DNA nicking to yield the open-circular form. The nicking activities of the phenothiazines were in the order: CPZ greater than PMZ greater than MQZ. CPZ elicited extensive degradation of the DNA by photosensitization. The nicking activities of the benzothiadiazines and AQ were much weaker than CPZ and PMZ.

Benzothiadiazines↗

PubMed1987

Liquid chromatographic screening of diuretics in urine.

We describe a liquid chromatographic screening procedure for the detection, in urine, of twelve of the fifteen potassium-depleting diuretics available in Australia. A 2-ml urine sample was acidified with NaH2PO4 (pH 4.1) and extracted with 4 ml ethyl acetate. The sample was cleaned up further by washing with 5 ml Na2HPO4 (pH 7.5). The ethyl acetate was then evaporated to dryness, the residue reconstituted in 100 microliters mobile phase and 5 microliter were injected onto a Merck LiChrosorb RP-18 (5 microns) column. The ultraviolet absorbance of the eluent was monitored at 271 nm for 10 min. The screen was evaluated by giving each of thirty volunteers the lowest recommended dose of one of the diuretics in the study and obtaining urine samples 4, 8 and 24 h after having taken the dose. Twelve diuretics, chlorothiazide, hydrochlorothiazide, quinethazone, chlorthalidone, methyclothiazide, clopamide, frusemide, metolazone, mefruside, bendrofluazide, cyclopenthiazide and bumetanide, were all detectable up to 24 h after a dose. We therefore conclude that the screen would be reliable for the detection of these diuretics in urine.

Chromatography, High Pressure Liquid↗

PubMed1987

Magnesuria induced by thiazides and the influence of triamterene.

The effects on magnesium excretion of 4 short-term diuretic treatments (methyclothiazide 2 mg either alone or associated with increasing doses of triamterene) were evaluated in 8 normal volunteers and compared to spontaneous variations during placebo administration. The thiazide exerted a small but significant magnesuric effect, which was prevented only by the lowest dose (25 mg) of triamterene. Larger doses had no protective effect on thiazide-induced magnesuria. Independently of their absolute effects on magnesium excretion, all diuretics impaired the normal ability of the kidneys to compensate fully for the expected changes in magnesium reabsorption induced by extracellular volume contraction.

Adult↗

PubMed1988

Diuretic-induced CNS magnesium alteration and digoxin intoxication.

Male Wistar rats were injected intraperitoneally for 3 consecutive days with hydrochlorothiazide (HCTZ; 15 mg/kg), chlorothiazide (CTZ; 100 mg/kg), bendroflumethiazide (BFTZ; 1.5 mg/kg), chlorthalidone (CHLOR; 15 mg/kg), methyclothiazide (METH; 1.0 mg/kg) or metolazone (MET; 1.5 mg/kg). Magnesium content was measured in the hypothalamus, medulla oblongata, cerebral cortex, heart, skeletal muscle and serum. Although there was no consistent alteration of Mg in the serum, skeletal muscle and heart, there was a significant effect on hypothalamic and medullary Mg. Compared to a control value of 17.20 +/- 1.24 mEg/kg in the hypothamus there was a decrease by HCTZ (26%; p less than 0.01), CTZ (24%; p less than 0.01) and BFTZ (30%; p less than 0.01). Similarly, there was a decrease by HCTZ (22%; p less than 0.01), CTZ (30%; p less than 0.01) and BFTZ (25%; p less than 0.01) on Mg in medulla. In contrast MET increases Mg in hypothalamus (31%; p less than 0.01) and medulla (26%; p less than 0.01). Furthermore, digoxin infusion (0.051 ml/min) in animals pretreated with HCTZ induced arrhythmias earlier than in animals receiving digoxin alone (30 vs. 60 min; p less than 0.01). The effects of digoxin toxicity in HCTZ-pretreated animals were partially reversed by CNS administration of 50 micrograms of Mg. These findings strongly suggest that thiazide-induced depletion of Mg in the CNS predisposes to digoxin intoxication.

Animals↗

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↗

PubMed1965