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PubMedDate not supplied

Detection of alpha-methyldopa on thin-layer plates using pi-acceptors in 1,4-dioxane.

pi-Acceptors (P-chloranil and chloranilic acid) in 1,4-dioxane were used to detect alpha-methyldopa on thin layer plates. Thin layer plates coated to a thickness of 0.25 mm with silica gel G60 were spotted with solution of alpha-methyldopa from drug formulations and pure alpha-methyldopa solution. The plates were developed in a solvent system of methanol: glacial acetic acid: water (14:5:3). The developed plates were dried and sprayed with pi-acceptors, and further were counter-sprayed with dimethylformamide (DMF). P-Chloranil gave an immediate blue green complex with alpha-methyldopa which intensified on counter-sprayed with DMF. alpha-methyldopa (reference sample and those from drug formulations) gave Rf of 0.85 and excipients from the drug formulations did not interfere with the result.

Benzoquinones↗
PubMed1976

Alpha-methyldopa interference with the phosphotungstate uric acid test.

The effect of alpha-methyldopa on the phosphotungstate method of uric acid analysis was tested using a group of 17 hypertensive patients being treated with only this drug for their elevated blood pressure. The uric acid values of these patients tested by the phosphotungstate method showed no significant difference from the uricase test values, when compared to a control population of 32 normotensive patients tested in the same manner. The proposed interference was further tested by in vitro studies. Both uricase and phosphotungstate analysis of uric acid was performed on serum containing various dilutions of alpha-methyldopa. The concentration of alpha-methyldopa required to clinically affect the uric acid level, whereby a false positive result occurred, was 60 mug/ml. The mean plasma aplha-methyldopa concentration in the study group, however, was found to be only 2.03 mug/ml. The postulated interference of therapeutic levels of alpha-methyldopa on the phosphotungstate uric acid method was invalid.

Adult↗
PubMed1991

[A comparative study of nisoldipine and alpha-methyldopa in aged patients with isolated systolic hypertension].

A comparative, randomized and cross clinical trial between nisoldipine and alpha-methyldopa in 50 aged patients with isolated systolic hypertension during 12 weeks. The therapeutic aim (SAP less than or equal to 160 mmHg) was reached after the first period in the 60% of the patients treated with nisoldipine and the 63% of those who took alpha-methyldopa (ns), and after the second period: 77% in nisoldipine group and 82% for alpha-methyldopa (ns). Adverse effects were experienced in the 21.7% of the patients treated with nisoldipine and in the 60.8% of the patients who received alpha-methyldopa (p less than 0.001. Nisoldipine had a lower effect that alpha-methyldopa over the diastolic arterial pressure. It was not any change in the biochemical parameters related to both antihypertensive drugs.

Age Factors↗
PubMed1986

Ketanserin compared to nifedipine and methyldopa in patients aged above 50 years: two international multicentre studies. For the International Study Group.

The antihypertensive properties and adverse reactions of ketanserin, nifedipine and methyldopa were compared in hypertensive patients aged above 50 years in two international studies. After a placebo run-in period, patients received for 3 months, either ketanserin or nifedipine retard in study 1, and either ketanserin or methyldopa in study 2. After 1 month of monotherapy, a diuretic was added if necessary. Study 1 had 117 subjects, with 119 in study 2. The changes in systolic and diastolic blood pressure were similar for ketanserin and nifedipine although more patients switched to combination therapy in the ketanserin group. The overall response rate was comparable with ketanserin and nifedipine (96% for both drugs). The decrease in diastolic blood pressure was significantly greater in the ketanserin group compared to methyldopa and more patients responded to ketanserin (82%) than to methyldopa (65%). No rebound hypertension was observed on discontinuation of therapy with any of the drugs. The total incidence of adverse reactions in monotherapy was lower with ketanserin than with nifedipine (34 and 47%) and similar for ketanserin and methyldopa (40 and 45%). For ketanserin no consistent adverse reaction pattern was seen.

Blood Pressure↗
PubMed1986

Comparative evaluation of captopril and methyldopa monotherapy for hypertension: double-blind study in Indians.

A double-blind, parallel-group study was conducted in 41 Indian men and women with hypertension to compare the antihypertensive effects of captopril and methyldopa. Twenty patients received 150 mg of captopril and 21 patients received 750 mg of methyldopa daily. The drugs were administered in three equally divided doses for four weeks. Blood pressure was measured after one, two, and four weeks of therapy. Relevant clinical and biochemical investigations were carried out before and after treatment. Sixteen patients given captopril and 11 given methyldopa responded to therapy. Among the captopril responders, initial mean systolic blood pressure (+/- SE) was 155 +/- 5.0 mmHg and diastolic blood pressure was 105 +/- 2.1 mmHg. These values were reduced to 119 +/- 9.8 and 80 +/- 6.1 mmHg, respectively, after four weeks of therapy. Similarly, among the methyldopa responders, initial mean systolic blood pressure was 180 +/- 7.4 mmHg and diastolic blood pressure was 112 +/- 3.8 mmHg. These values were reduced to 138 +/- 7.0 and 92 +/- 3.8 mmHg, respectively, after four weeks of therapy. The fall in the blood pressure in both groups was highly significant (P less than 0.001). None of the patients in either group had any clinically significant side effects. The results of this study suggest that monotherapy with captopril may be more effective than monotherapy with methyldopa in Indian hypertensives.

Captopril↗
PubMed1987

Intestinal absorption of alpha-methyldopa: in vitro mechanistic studies in rat small intestinal segments.

The mechanism of intestinal uptake of alpha-methyldopa (Aldomet) was investigated using isolated segments of rat small intestine. Incubations were limited to 2 to 5 min as histological examination of the tissue showed significant loss of structural integrity after 10 to 20 min at 37 degrees C. alpha-Methyldopa in the tissue was extracted and assayed by high-pressure liquid chromatography. Corrections were applied for uptake into extracellular spaces using inulin (14C). Uptake was temperature- and concentration-dependent (Km congruent to 10 mM), was dependent on the location in the small intestine and was inhibited by ouabain (2 mM) or lack of sodium or glucose in the incubation medium. alpha-Methyldopa uptake also was inhibited by other neutral amino acids. The mucosal cell layer accounted for approximately 50% of the total drug accumulated in the tissue. Uptake was less when the serosal surface was exposed than when the tissue was everted. The similarity in uptake parameters between alpha-methyldopa and L-phenylalanine (parallel experiments) suggests that alpha-methyldopa is principally absorbed into rat small intestinal mucosal cells via an amino acid transport system.

Amino Acids↗
PubMed1979

Methyldopa abolishes neurally evoked contractions of the vas deferens in vitro.

Low concentrations of methyldopa (2 microgram/ml - 20 microgram/ml) reduced neurally evoked contractions of the isolated guinea-pig and the rat vas deferens. These contractions were completely abolished when the vas was incubated with methyldopa (200 microgram/ml - 400 microgram/ml) for 1.5 hr +/- 0.1 hr (guinea-pigs) and 3.0 hr +/- 0.5 hr (rats). Vasa deferentia incubated with methyldopa became supersensitive to noradrenaline and dopamine. Vas deferentia from reserpinized animals showed reduced contractions upon electrical stimulation but became supersensitive to dopamine and noradrenaline. Reserpine pretreatment diminished the response of the vas to tyramine; however, methyldopa restored the responses to a greater magnitude suggesting the formation of methyldopamine and methylnoradrenaline. The possible mechanisms of action of methyldopa is discussed.

Animals↗
PubMed1978

Urinary free methyldopa determined by reversed-phase high-performance liquid chromatography.

We describe a chromatographic method, in which 3,4-dihydroxybenzylamine is used as the internal standard, for determining free methyldopa in human urine. The drug was adsorbed onto alumina, eluted, and the eluate directly injected onto a reversed-phase column (octadecyl-bonded silica stationary phase), with dilute acetate buffer (pH 2.7) as the mobile phase and ultraviolet detection at 280 nm facilitated. Methyldopa is well separated from other urinary biogenic amines present in the alumina extract, and other commonly used antihypertensives and diuretics do not interfere with the analysis. The sensitivity of the method is adequate to quantify 8.0 mg of methyldopa per liter in 30 ml of sample; the lower limit of detection is 25 ng. Analytical recovery for methyldopa varied from 95 to 102% with within-run and day-to-day coefficients of variation of 2.7 (n = 10) and 3.8% (n = 5), respectively. This procedure is readily adaptable for use in studies of the pharmacokinetics of methyldopa and to routine clinical laboratory use.

Adult↗
PubMed1983

A comparison of timolol plus hydrochlorothiazide plus amiloride and methyldopa in essential hypertension in Black Africans.

The antihypertensive effect of the fixed combination of timolol, a beta-blocking agent, hydrochlorothiazide, a thiazide diuretic, and amiloride, a potassium sparing agent, was compared against that of methyldopa in an open study lasting 16 weeks in 32 ambulatory African patients with previously untreated diastolic blood pressure of 95-120 mm Hg. A significant fall in mean diastolic and systolic blood pressure was achieved in both groups up to 8 weeks of treatment and was sustained in the timolol-hydrochlorothiazide-amiloride group during the entire follow-up. In the methyldopa group, mean diastolic and systolic blood pressure rose during follow-up. At 16 weeks the fall in mean diastolic and systolic blood pressure was significantly greater in the timolol-hydrochlorothiazide-amiloride treated patients than in the methyldopa group. Adverse reactions were more frequent and severe in the methyldopa group than in timolol-hydrochlorothiazide-amiloride treated patients. It is concluded that the fixed drug combination of timolol-hydrochlorothiazide-amiloride (Moducren) is effective in controlling mild to moderate hypertension in Africans and is better tolerated than methyldopa in these patients. It is further noted that hypertensive patients can be treated with a combination tablet once a day. This is of crucial significance as it would promote better compliance and, hence, minimize the sequelae of poorly controlled hypertension.

Adult↗
PubMedDate not supplied

Effect of alpha-methyldopa on lung microembolism in the rat.

The effect of chronic pretreatment with alpha-methyldopa on acute pulmonary hypertension induced by lung microembolization with Sephadex particles in the rat was studied. Alpha-methyldopa was administered twice a day for 10 days by oesophageal gavage (20 mg X kg-1 of body weight) prior to embolization. Rats were anaesthetized with urethane. A catheter was positioned in closed chest rats in the pulmonary artery and 50 microliter of Sephadex suspension in saline were injected. The control group was not pretreated with alpha-methyldopa. In a subgroup of control and pretreated rats, the cardiac output was measured by the dye dilution technique before and after lung microembolization. Rats pretreated with alpha-methyldopa had less pulmonary hypertension, higher cardiac output and more severe arterial hypoxaemia 15 min after lung microembolization than untreated animals. There was no difference in platelet counts prior and after embolization. We suggest that pulmonary hypertension after lung microembolization in the rat includes a vasoconstrictor component which can be suppressed by alpha-methyldopa, and that severe arterial hypoxaemia in pretreated rats is probably the result of a decrease of the ventilation/perfusion ratio in unobstructed areas, which in untreated rats may be prevented by active vasoconstriction.

Animals↗
PubMedDate not supplied

Protective action of methyldopa against ouabain-induced cardiac arrhythmias and lethality.

Methyldopa (25, 50 and 100 mg/kg, i.p.) was studied for its effect on cardiac arrhythmias and lethality induced by slow intravenous infusion of ouabain in guinea-pigs. Methyldopa increased the dose of ouabain required to elicit the arrhythmic stages and lethality. However, it did not provide any protection in reserpinized guinea-pigs. Methyldopa also inhibited the rate of the ouabain-induced rise in blood pressure and the peak pressor response. Yohimbine significantly antagonized the protective action of methyldopa. It is concluded that the protective action of methyldopa against the arrhythmogenic and lethal effects of ouabain may be due to its action on the indirect neural components of ouabain toxicity, mediated through stimulation of alpha 2-adrenoceptors.

Animals↗
PubMed1977

Comparison of trimazosin and methyldopa in hypertension.

Eighteen patients with hypertension participated in a double-blind, randomized study to evaluate the effect of trimazosin, methyldopa, and placebo on supine and standing blood pressure and heart rate. Of 6 patients on methyldopa, one developed drug fever (and was dropped from the study) and one developed impotence. None of 6 patients on trimazosin and none of 6 patients on placebo developed any adverse effects. The mean supine blood pressure on 900 mg trimazosin daily was 17.0/12.8 mm Hg lower than that on the first placebo trial (p less than 0.01) and 17.0/12.1 mm Hg lower than that on the second placebo trial (p less than 0.01). The mean supine blood pressure on 2,250 mg methyldopa daily was 17.8/12.4 mm Hg lower than that on the first placebo trial (p less than 0.01) and 16.8/13.0 mm Hg lower than that on the second placebo trial (p less than 0.01). The mean supine blood pressure was not significantly affected by placebo. Trimazosin, 900 mg daily, and methyldopa, 2,250 mg daily, were equally effective in lowering supine and standing systolic and diastolic blood pressure and did not affect supine or standing heart rate.

Blood Pressure↗
PubMed1979

Prazosin in hypertension with and without methyldopa.

The efficacy of prazosin was assessed in 21 patients with essential hypertension who failed to respond adequately to a combination of methyldopa and hydrochlorothiazide. The patients were divided randomly into two groups; in the first group prazosin was substituted for methyldopa and in the second group prazosin was added to the combination. In group 1, the average blood pressure (BP) fell from 144/102 mmHg (sitting) and 142/105 mmHg (standing) to 136/91 mmHg (sitting) and 129/91 mmHg (standing) after prazosin (17 mg) was substituted for methyldopa. The fall in the diastolic BP was statistically significant (p less than 0.01). In group 2, BP fell from 146/101 mmHg (sitting) and 143/103 mmHg (standing) to 126/87 mmHg (sitting) and 118/86 mmHg (standing) when prazosin 14 mg was added to methyldopa and hydrochlorothiazide. The reductions in systolic and diastolic pressures were statistically significant (p less than 0.001).

Adult↗
PubMed1980

Methyldopa produces central inhibition of parasympathetic activity in the cat.

alpha-Methyldopa (10-100 mg/kg i.v.) produced a dose-dependent pupillary dilation in anaesthetized cats which was antagonized by subsequent administration of yohimbine hydrochloride (0.5 mg/kg i.v.). The peak effects were observed approximately 2-3 h after injection. This alpha-methyldopa-induced mydriasis was present only when the parasympathetic innervation to the iris was intact. Prior treatment with yohimbine (0.5 mg/kg i.v.) 30 min before alpha-methyldopa also antagonized the mydriatic effect, whereas pretreatment with phenoxybenzamine (2.5 mg/kg i.v.) did not. In contrast, phenoxybenzamine, but not yohimbine, effectively antagonized the pupillary dilation produced by adrenaline (0.3-10.0 microgram/kg i.v.). These results suggest that alpha-methyldopa produces mydriasis in the cat by means of CNS inhibition of tonic outflow from the oculomotor nucleus and that an alpha-adrenergic inhibitory mechanism may be involved. This conclusion is supported further by experiments in which direct measurements of ciliary nerve activity were made.

Animals↗
PubMed1977

Dose-titrated, double-blind, cross-over comparison of a selective beta-blocker and methyldopa in the treatment of hypertension.

The efficacy and toxicity of tolamolol and methyldopa in hypertensive patients has been compared by a dose-titrated, double-blind, cross-over study. Thirteen patients completed the trial. Within the dose ranges investigated (tolamolol - 300 mg/day - 900 mg/day; methyldopa - 750 mg/day - 2250 mg/day)both drugs produced significant falls in laying and standing, systolic and diastolic blood pressures. Although the hypotensive effects of methyldopa were more marked than tolamolol, these only achieved conventional (P less than 0.05) levels of significance for lying blood pressure. There were no objective changes in haematological or biochemical indices during treatment with either drug, but patients complained of tiredness, weak limbs and mouth dryness significantly more during methyldopa treatment, than during either placebo or tolamolol therapy.

Adult↗
PubMed1983

Absence of an effect of mianserin on the actions of clonidine or methyldopa in hypertensive patients.

The concurrent administration of tricyclic antidepressants has been shown in man to result in a clinically significant impairment of the antihypertensive effect of clonidine. This interaction is thought to be related to competition for central alpha 2 receptors where clonidine acts as an agonist and the tricyclics act as antagonists. Although it seems to cause less cardiovascular effects than tricyclic antidepressants, the tetracyclic antidepressant, mianserin also has been reported to be an alpha receptor antagonist and may, therefore, also interfere with the antihypertensive activity of centrally-acting drugs. This study investigates the effects of acute and chronic mianserin administration in patients with essential hypertension established on long term treatment with either clonidine or methyldopa. The first dose of mianserin was not associated with an increase in blood pressure and during a further two weeks of mianserin therapy there were no significant alterations in blood pressure, supine or erect. Similarly, mianserin did not alter heart rate either after acute or after chronic administration. Mianserin itself had a sedative effect but there was no interference with the sedation attributable to clonidine or methyldopa. Mianserin caused no reduction salivary flow and did not influence the reduced saliva production caused by clonidine. Both clonidine and methyldopa are associated with a reduction in sympathetic outflow but there was no evidence in this study of any further change in plasma noradrenaline or 24 h urinary catecholamine excretion. This study demonstrates that if mianserin is given acutely or chronically, it does not interfere with the effects of the centrally acting anti-hypertensive drugs, clonidine and methyldopa. Mianserin may therefore be a suitable antidepressant for patients receiving these antihypertensive agents if drug treatment for depression is indicated.

Aged↗
PubMed1988

Effect of methyldopa on prolactin serum concentration. Comparison between normal and sustained-release formulations.

In a group of ten hypertensive patients, the effects of methyldopa administration in two different formulations on serum prolactin (PRL) were studied. A single oral dose of normal release methyldopa significantly increased serum prolactin levels, peak concentrations occurring 3 to 6 h after drug administration. On the contrary, administration of sustained release methyldopa at the same dose was only followed by slight and not significant fluctuations in prolactin plasma levels. Both formulations produced a significant decrease of systolic and diastolic blood pressures, without significant differences between sustained and normal release methyldopa effects.

Adult↗
PubMed1989

Sensitive colorimetric assay of carbidopa and methyldopa using tetrazolium blue chloride in pharmaceutical products.

A colorimetric method for the assay of carbidopa and methyldopa either in pure form or in pharmaceutical preparations is described. The method is based on the reduction of tetrazolium blue chloride in a non-aqueous alkaline medium by the substances analysed, and the measurement of the absorbance of the pink-coloured diformazan solution, which is caused by this reduction. The spectra of the aforesaid solutions exhibit an absorption maximum at lambda = 525 nm. The apparent molar absorptivities and Sandell's sensitivities (in l.mol-1.cm-1 and ng.cm-2, respectively) are 1.2.10(5) and 1.9 for carbidopa and 7.07.10(4) and 3.0 for methyldopa. The solution of diformazan formed obeys Beer's law in the concentration range of 0.05-4.0 ppm for carbidopa and 0.1-6.0 ppm for methyldopa. The slope and intercept of the corresponding regression line equation were obtained with a correlation coefficient of 0.9999 for carbidopa and 0.9994 for methyldopa. The variables affecting the development of the colour are investigated and the conditions are optimized. Compared with other procedures this method showed to be more simple and rapid, highly sensitive, precise and accurate. Results obtained by application of the proposed method and the official one, were in good agreement, while statistical comparison by the Student's t-test shows no significant difference between the two sets of the results.

Capsules↗