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PubMed1979

Atenolol and chlorthalidone on blood pressure, heart rate, and plasma renin activity in hypertension.

The antihypertensive effect of atenolol, with and without chlorthalidone, on hypertension was assessed in an outpatient as well as in an inpatient study. In the outpatient study atenolol alone induced decreases in systolic and diastolic BP amounting to 20 and 15 mm Hg. Maximal response of BP and HR developed within a week at the lowest dose used (100 mg twice daily). Combined atenolol-chlorthalidone treatment decreased lying and standing systolic BP by 7 and 14 mm Hg more than atenolol alone, but diastolic BP was decreased little more. In the inpatient study the addition of atenolol to chlorthalidone therapy in a dose of 100 mg twice daily resulted in a maximal decrease in BP within 3 days. At this dose PRA was lowered only slightly. Larger doses did not lead to any significant further decrease in BP, whereas PRA fell progressively. Our results indicate that, in contrast to nonselective blockade, specific beta-1-adrenoceptor blockade by atenolol is capable of inducing a distinct antihypertensive effect, unrelated to suppression of PRA. The decrease in PRA after larger doses of atenolol was not accompanied by a further decrease in BP. Because diuretic-induced renin release plays a role in the maintenance of the BP, our findings suggest that at higher dosages a hypertensive effect of the beta blocker compensated for the hypotensive effect of the decrease in PRA.

Adult↗

PubMed1978

Chlorthalidone-induced syndrome of inappropriate secretion of antidiuretic hormone.

A 60-year-old woman who had been instructed to increase her water intake because of nephrolithiasis developed the syndrome of inappropriate secretion of antidiuretic hormone when treated with chlorthalidone for mild hypertension. Serum osmolality was 235 mOsm/kg with concomitant urine osmolality of 490 mOsm/kg. When serum sodium decreased to 110 mEq/liter, plasma antidiuretic hormone (ADH) was elevated at 30 pg/ml. The syndrome resolved when chlorthalidone was discontinued together with fluid intake restriction. Plasma ADH returned to normal (less than 0.5 pg/ml) after three days of treatment. The favorable outcome in this patient is attributed to early recognition of the syndrome, which might occur even with nonthiazide diuretics such as chlorthalidone.

Chlorthalidone↗

PubMed1991

Influence of chlorthalidone on the pharmacokinetics and pharmacodynamics of Org 10172 (Lomoparan), a low molecular weight heparinoid, in healthy volunteers.

The influence of chlorthalidone (100 mg PO) on the pharmacokinetics and pharmacodynamics of Org 10172 (IV bolus injection of 3250 anti-Xa units), a low molecular weight heparinoid, was studied in six healthy male volunteers using an open randomized two-way crossover design. Chlorthalidone produced a slight decrease in clearance of anti-Xa activity from 7.1 +/- 1.0 to 6.6 +/- 0.8 mL/min and a decrease of the volume of distribution from 0.20 +/- 0.05 to 0.16 +/- 0.04 L/kg, whereas the volume of distribution of antithrombin activity increased from 0.14 +/- 0.05 to 0.26 +/- 0.10 L/kg (all differences P less than .05). During the entire study period no adverse events occurred. In summary, chlorthalidone showed separate effects on different fractions of Org 10172. The clinical implication of the slight change observed in plasma anti-Xa activity is likely to be limited, whereas the 80% increase in distribution volume of plasma antithrombin activity can not be defined as yet in terms of clinical relevance.

Adult↗

PubMed1983

Stability-indicating assay for chlorthalidone formulation: evaluation of the USP analysis and a high-performance liquid chromatographic analysis.

An investigation of the USP assay of chlorthalidone tablets showed that variable degradation of chlorthalidone occurred during assay preparation. The degradation products were isolated and identified. A stability-indicating high-performance liquid chromatographic (HPLC) assay which separates the degradation products from chlorthalidone was developed and used to examine the present USP preparation. The HPLC assay is suggested as an alternate.

Chlorthalidone↗

PubMed1987

Metabolic effects of long-term therapy with muzolimine and chlorthalidone in hypertension.

Previous short-term studies of muzolimine (a diuretic with frusemide-like activity) had shown that it did not induce a significant change in the serum potassium concentration. In the present study sodium and potassium handling and other metabolic variables have been compared during 16 weeks of therapy with muzolimine and chlorthalidone, a thiazide-like diuretic. During muzolimine treatment, plasma and red cell potassium concentrations remained unchanged, while a significant fall in potassium occurred with chlorthalidone. Neither drug affected the activity of sodium-potassium cotransport or sodium-lithium countertransport in red cells in vitro. Muzolimine and chlorthalidone had similar effects on arterial pressure and on the other metabolic variables tested.

Adult↗

PubMed1984

Changes in left ventricular mass during a double-blind study with chlorthalidone and slow-release nifedipine.

The presence of a possible correlation between changes in left ventricular mass of hypertensive patients and the degree of blood pressure reduction with different antihypertensive drugs has been investigated in 40 outpatients by M-mode echocardiography. Ten of these, with blood pressure in normal limits with different antihypertensive treatment had their therapy changed in chlorthalidone 25 mg/day without any run-in (Group A); other 30 patients, with a previously uncontrolled blood pressure, after a 14 day run-in, were randomly allocated to chlorthalidone 25 mg/day (Group B), slow release nifedipine 20 mg/day (Group C) or placebo (Group D). At the end of the eight week treatment period a further decrease in systolic blood pressure was observed in Group A without changes in ventricular mass; an highly significant decrease in both systolic and diastolic blood pressure was observed in B and C but only patients on chlorthalidone changed their ventricular mass; no change in both blood pressure and ventricular mass was observed on placebo. As changes in ventricular mass are not correlated with blood pressure reduction, we conclude that other, not well defined factors, apart from the decrease in duration and degree of left ventricular systolic wall tension, may be responsible for reversal of left ventricular hypertrophy.

Adult↗

PubMed1978

Placental transfer of chlorthalidone and its elimination in maternal milk.

A gas chromatographic method has been used to determine chlorthalidone in amniotic fluid, maternal and foetal blood at delivery, and in maternal milk and blood three days after delivery, following the administration of chlorthalidone to nine pregnant women suffering from toxaemia of pregnancy. Placental transfer of chlorthalidone and elimination in maternal milk have been shown and the implications of these factors are discussed. An explanation has been proposed for our observations that foetal blood levels of the drug are about 15% of those in maternal blood.

Amniotic Fluid↗

PubMed1975

Comparison of the antihypertensive effect of propranolol and practolol combined with chlorthalidone.

A double blind cross-over trial of fixed doses of propranolol (640 mg/day) and the cardioselective drug practolol (1600 mg/day) was performed in 28 patients with essential hypertension whose blood pressure was not adequately controlled by chlorthalidone (100 mg 3 times weekly) alone. Chlorthalidone alone was given during the first (control) period, and it was continued throughout the propranolol and practolol treatment periods, each of 10 weeks. The systolic and diastolic blood pressures were lowered significantly by both the beta blocking drugs. The changes in blood pressure caused by altering the patient's position were the same after both beta blockers. Propranolol produced slightly lower values than practolol, but the difference was significant only for diastolic blood pressure in the sitting and supine positions. In individual patients the final blood pressure after propranolol was correlated with the final blood pressure after practolol. Only minimal side-effects of either drug were noticed. It is concluded that the doses employed both of propranolol and practolol had a good and approximately equal antihypertensive effect when combined with chlorthalidone treatment. There was no correlation between the final blood pressure and plasma renin activity.

Antihypertensive Agents↗

PubMed1985

Beneficial effects from systematic dosage reduction of the diuretic, chlorthalidone: a randomized study within a clinical trial.

The purpose of this study was to determine the effects on blood pressure and selected biochemical measures of reducing the dosage of chlorthalidone from 100 mg to 50 mg. Within the larger study (Multiple Risk Factor Intervention Trial), 140 Special Intervention hypertensive men, taking 100 mg of chlorthalidone daily, were randomly assigned to either a continuation of 100 mg or a dosage reduction to 50 mg daily. Men were followed monthly for 4 months. Measures were made of blood pressure, serum potassium, serum uric acid, serum glucose, serum cholesterol, and triglycerides. Blood pressure change from baseline to 4 months revealed a significantly higher diastolic blood pressure in the group continued on the 100 mg dose compared to the dose reduction group. However, analysis of covariance, which took into account baseline differences in blood pressure, resulted in a nonsignificant difference in follow-up blood pressure (systolic and diastolic) between groups. Serum potassium increased significantly in the dose reduction group, especially in those participants taking supplemental potassium chloride. The results of this study demonstrate that a reduced dose of 50 mg chlorthalidone over the 4-month period was as effective as the 100 mg dose in long-term, well-controlled hypertensive men. Careful study of other antihypertensive agents is warranted to determine the drug dose that is maximally effective for blood pressure lowering and that also minimized toxic and adverse effects.

Blood Glucose↗

PubMed1980

The effect of chlorthalidone on serum lipids and lipoproteins.

The effect of chlorthalidone treatment on serum lipids and lipoproteins was investigated in 21 hypertensive patients. Chlorthalidone caused an increase in total serum and low density lipoprotein (LDL) cholesterol, but not in high density lipoprotein (HDL) cholesterol. Serum and lipoprotein triglycerides also increased. Our findings suggest that chlorthalidone increases serum concentrations of "atherogenic" lipoproteins (LDL and VLDL), and possibly decreases the levels of a "beneficial" lipoprotein, namely HDL. Thus, the use of this medication may increase a major atherosclerosis risk factor.

Adult↗

PubMed1980

Increased serum low-density lipoprotein cholesterol in men treated short-term with the diuretic chlorthalidone.

The effect of the diuretic chlorthalidone (100 mg/day for 6 weeks) on serum lipoproteins was evaluated in 37 subjects. In 19 men with essential hypertension (aged 41 +/- 3 yr), 8 normal men (26 +/- 3 yr), or all of these men considered together, chlorthalidone significantly increased serum low density lipoprotein--cholesterol (LDL-C) by 20% (p less than 0.05 to less than 0.01). There was also a tendency for increased LDL-C in seven postmenopausal women (+/- 15%) but not in three premenopausal women with essential hypertension. High density lipoprotein--cholesterol was not significantly changed in hypertensive women or normal men and decreased slightly (p less than 0.05) in hypertensive men. Apolipoproteins A-I, A-II, and B were not changed significantly in women or men. Diuretic-induced lipoprotein alterations were not associated with altered plasma volume and unrelated to variations in serum potassium, glucose, insulin levels, blood pressure, and body weight. Short-term diuretic therapy with chlorthalidone may increase serum LDL-C in young or middle-aged men with normal or high blood pressure.

Adolescent↗

PubMed2000

Chromatographic separation of chlorthalidone enantiomers using beta-cyclodextrins as chiral additives.

Different beta-cyclodextrins have been tested as chiral additives in the mobile phase for the chromatographic analysis of chlorthalidone enantiomers in a C18 LiChrospher (125 x 4 mm I.D.) column. The effect on enantioresolution of different parameters was studied: composition of the mobile phase (percentage of organic solvent, type of buffer and pH), mobile phase flow-rate, and type and concentration of beta-cyclodextrin. A 25:75 mixture of methanol and 0.1 M phosphate buffer, pH 4, containing 2% triethylamine (v/v), and 12.5 mM beta-cyclodextrin, at a flow-rate of 0.8 ml/min, was found to be the best option for the resolution of chlorthalidone enantiomers. Under such conditions, linear calibration curves were obtained in the 0.5-20-microg/ml interval using UV detection at 230 nm. The limit of detection for both isomers was 50 ng/ml. The utility of the described assay has been tested by analyzing chlorthalidone in different pharmaceutical preparations. Examples of application to biological samples are also given.

Chlorthalidone↗

PubMed1997

Simultaneous determination of atenolol and chlorthalidone in plasma by high-performance liquid chromatography. Application to pharmacokinetic studies in man.

An HPLC method developed to detect in a single run both atenolol and chlorthalidone, extracted from plasma, using two detectors (UV for chlorthalidone and fluorometric for atenolol) connected in series, is described. The drugs were separated on an ODS column at room temperature using a 0.05 M sodium dodecyl sulphate in phosphate buffer (pH 5.8)-n-propanol (95:5, v/v) solution, delivered at a flow-rate of 1.3 ml/min. Having ascertained the sensitivity (10 ng/ml of both drugs) and the intra-day reproducibility (pre-study validation), the reliability of the method was verified by inter-day assays (within-study validation) carried out during the analysis of plasma samples collected from healthy volunteers after single-dose treatment with atenolol+chlorthalidone tablets (pharmaceutical preparations containing 100+25 mg and 50+12.5 mg of the two drugs, respectively).

Antihypertensive Agents↗

PubMed1983

Antihypertensive mechanism of diuretic treatment with chlorthalidone. Complementary roles of sympathetic axis and sodium.

Twenty-three patients with untreated mild to moderate essential hypertension had on the average an abnormally increased cardiovascular pressor responsiveness to exogenous norepinephrine (NE), while plasma and urinary NE, exchangeable body sodium and blood volume were normal. An increased pressor responsiveness to angiotensin II in these patients was associated with a tendency for low plasma renin activity (PRA). Compared to placebo conditions, treatment with chlorthalidone, 100 mg/day, for 6 weeks significantly decreased blood pressure and exchangeable sodium in these hypertensive patients but not in ten normal subjects; blood volume and heart rate were unchanged in both groups. Chlorthalidone induced a marked increase in PRA, but only a mild increase in angiotensin II pressor dose. In contrast, the diuretic caused a greater increase in NE pressor dose than in plasma NE in the hypertensive group, thus improving the disturbed relationship between plasma NE and NE responsiveness in these patients. No significant modification of plasma NE and NE responsiveness occurred in diuretic-treated normal subjects. In addition to sodium and the renin-angiotensin system, the sympathetic regulatory axis seems to be involved in the antihypertensive mechanism of chlorthalidone. Thiazide-like diuretics may decrease blood pressure in essential hypertension in part by lowering an abnormally high cardiovascular NE responsiveness without causing an equivalent increase in circulating NE.

Adult↗

PubMed1983

Determination of chlorthalidone and clonidine hydrochloride in tablets by HPLC.

A rapid, reversed-phase high performance liquid chromatographic method is described for the determination of chlorthalidone and clonidine hydrochloride combinations in tablets. Individual tablets or composite samples were sonicated in water, diluted with methanol, and filtered prior to chromatographing. Chlorthalidone, formulated at 15 mg/tablet, was chromatographed on octadecylsilyl-bonded, 5 to 6-micrometers, spherical silica with 50% methanol in water mobile phase. Clonidine hydrochloride, formulated at 0.1 or 0.2 mg/tablet, was chromatographed on trimethylsilyl-bonded, 5 to 6-micrometers, spherical silica with 65% methanol in pH 7.9 phosphate buffer mobile phase. Both were determined with a spectrophotometric detector at 254 nm. Mean recoveries of the drugs from six synthetic tablet samples were 100.3% for chlorthalidone and 99.7% for clonidine hydrochloride (at 0.1 mg/tablet level) with coefficients of variation of 0.79 and 1.55%, respectively.

Chlorthalidone↗

PubMed1992

The treatment of obese hypertensive black women: a comparative study of chlorthalidone versus clonidine.

OBJECTIVE: We attempted to determine a valid pharmacological approach for the control of high blood pressure in obese hypertensive patients using two antihypertensive agents with different pharmacological actions. DESIGN: Thirty-two obese hypertensive black women were randomly treated with chlorthalidone or clonidine to achieve adequate blood pressure control. Unresponsive patients received combination therapy with both agents. RESULTS: Twenty-nine patients completed the study. Systolic and diastolic blood pressures were reduced with both agents, more so with chlorthalidone. Of the 15 patients treated with chlorthalidone, 14 had satisfactory reduction in diastolic pressure compared with only four of the 14 treated with clonidine. Of the 11 unresponsive patients treated with combination therapy, 10 achieved satisfactory control of blood pressure. CONCLUSIONS: We conclude that a rational approach to the treatment of hypertension in obese black women includes diuretics, a first choice attempt that tries to address the hemodynamic alterations previously identified in those patients. Combining diuretics with an alpha-adrenergic agonist resulted in complete control of blood pressure in most of the hypertensive patients in our study. The lowest dose of each antihypertensive medication, especially when used in combination, was effective in a high percentage of patients. The use of this antihypertensive approach also helps to clarify which of the underlying pathophysiological mechanisms should be targeted when other currently available antihypertensive medications are used.

Black People↗

PubMedDate not supplied

Effects of antihypertensive agents propranolol, metoprolol, nadolol, prazosin, and chlorthalidone on ACAT activity in rabbit and rat aortas and on LCAT activity in human plasma in vitro.

Various antihypertensive agents were studied in vitro to determine their effects on cholesterol esterification by arterial ACAT (acylCoA:cholesterol acyltransferase; E.C. 2.3.1.26) and on the activity of plasma LCAT (lecithin:cholesterol acyltransferase; E.C. 2.3.1.43). Propranolol inhibited ACAT in normal rat aorta, atheromatous rabbit aorta, and in isolated microsomes from atheromatous rabbit aorta, and in isolated microsomes from atheromatous rabbit aorta. Inhibition reached 50% in microsomes at approximately 0.8 mM. Metoprolol, prazosin, and chlorthalidone also inhibited microsomal ACAT, but to a lesser extent than propranolol; nadolol had no effect on the enzyme. Propranolol, metoprolol, prazosin, and chlorthalidone also inhibited LCAT in human plasma, whereas nadolol showed no inhibitory effect. Fifty percent inhibition occurred at 2 mM with prazosin and chlorthalidone and at 4-5 mM with propranolol. Metoprolol showed a weak dose-dependent inhibition that ranged from 2 to 10% over the concentration range 0.5-5 mM. The data suggest a mechanistic basis for altered lipoprotein profiles observed clinically with certain antihypertensive therapies and suggest that a direct effect of beta-blockers on arterial wall metabolism may account for their recognized ability to reduce the development of experimental atherosclerosis and to improve survival in post-myocardial infarction patients.

Adult↗

PubMed1987

Enalapril in essential hypertension: the comparative effects of additional placebo, nicardipine and chlorthalidone.

The effect of adding placebo, a calcium antagonist, nicardipine and a thiazide diuretic, chlorthalidone, each for 2 weeks, to ongoing treatment with the ACE inhibitor, enalapril was evaluated in seven patients with essential hypertension. Compared with placebo, nicardipine and chlorthalidone both significantly enhanced the antihypertensive effect of enalapril: average blood pressure reductions over 8 h were respectively 26/16 and 33/17 mm Hg (supine) but the time-course of these augmented effects was significantly different. In particular, blood pressure control with the addition of nicardipine, despite apparently being at steady state, was significantly attenuated during the latter part of the dosage interval and therefore was less well sustained at 24 h. In contrast, an effect throughout 24 h appeared possible with the chlorthalidone-enalapril combination.

Acetylcholinesterase↗