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At least 19 recordsLinked to original sources
PubMedDate not supplied

Bethanidine dose, plasma levels, and antihypertensive effects.

Bethanidine dose, plasma levels, and hypotensive effects were evaluated in twelve hypertensive patients. Diuretic therapy with benzthiazide was started two weeks before and continued during the study. Bethanidine was given three times daily. After two to 12 months of therapy in 11 of the patients, the mean standing diastolic pressure was reduced from 112 to 91 mm Hg. The mean total daily bethanidine dose was 79 mg (range 30--150 mg). The mean plasma bethanidine was 0.65 micrometer (range 0.1--2.8 micrometer), which correlated with the bethanidine dose. There was less correlation between dose and antihypertensive effect. The effects of sudden withdrawal from chronic bethanidine dosing were observed in six patients. The orthostatic effect of bethanidine was lost within 12 hours, but the half-time of elimination of bethanidine from plasma was 39 hours. Based upon the present findings, recommendations are presented for initiation and maintenance of antihypertensive therapy with bethanidine.

Adult↗
PubMed1977

Multiclinic controlled trial of bethanidine and guanethidine in severe hypertension.

One hundred and eight patients with initial diastolic blood pressure in the range of 100-124 mm Hg while taking hydrochlorothiazide were assigned randomly and double-blind to hydrochlorothiazide plus either bethanidine or guanethidine. The average reduction of the fifth and sixth months' diastolic blood pressure was 18.4 mm Hg for guanethidine and 13.6 mm Hg for bethanidine (P less than 0.01). The distribution of the individual values was such that 68.8% of guanethidine treated patients achieved a diastolic level below 90 mm Hg, compared to only 45.5% of the bethanidine treated group (P less than 0.025). The degree of orthostatic fall in blood pressure was greater with bethanidine than with guanethidine (P less than 0.05). The diurnal variation of blood pressure was slightly greater with bethanidine than with guanethidine. The results significantly favor guanethidine. This study failed to demonstrate that the shorter action of bethanidine confers significantly better control of blood pressure than the longer action of guanethidine.

Bethanidine↗
PubMed1975

Fluorometric assay of bethanidine in plasma.

A fluorometric method for determining bethanidine in blood plasma is described. The bethanidine is extracted into chloroform, a drug-dye complex with eosin Y is formed, and the fluorescence is measured (excitation, 535 nm; fluorescence, 560 nm). The assay detects 0.02 muM bethanidine (4 ng/ml) in plasma. The relative fluorescence of several body constituents and antihypertensive drugs is negligible. The plasma levels of bethanidine in four hypertensive patients receiving this drug were measured.

Animals↗
PubMed1979

A comparison and an investigation of a potential synergistic effect of labetalol and bethanidine in patients with mild hypertension.

1 The effects of labetalol, bethanidine and combined treatment with both drugs were compared in a within-patient randomized cross-over study in mild essential hypertension. Attention was directed to whether or not labetalol and bethanidine differed in their pattern of effect on arterial BP and whether evidence of synergism was apparent. 2 At the doses used labetalol significantly lowered systolic and diastolic BPs and heart rate lying, sitting, standing and after exercise. The dose of bethanidine used did not affect heart rate significantly while lowering systolic and diastolic BPs only after exercise and less clearly on standing. Combined treatment lowered BPs on standing and after exercise and heart rate after exercise. 3 The type and frequency of side-effects were similar with bethanidine and labetalol but were much less with combined treatment. 4 No evidence of synergism was observed.

Adult↗
PubMedDate not supplied

Bethanidine elimination from plasma.

Bethanidine was administered intravenously to six hypertensive patients with normal renal function and five hypertensive patients with renal impairment. After administration of 0.7 mumole/kg, blood was sampled at frequent intervals for measurement of plasma bethanidine. The plasma levels were analyzed on a three-compartment exponential open-model system. The second rapid elimination phase (beta) had a half-time of 3.4 hours in normal subjects and was insignificantly prolonged to 16.4 hours in renal impairment. There was an extended terminal elimination phase of 90 and 70 hours for normals and impaired, respectfully. The volume of distribution at pseudoequilibrium was 2.8 and 1.6 liters/kg, respectively, suggesting significant sequestration of the drug in body tissues. The pharmacokinetic constants of bethanidine in normal and impaired renal functions were similar.

Adult↗
PubMed1976

A within-patient comparison of bethanidine, methyldopa and propranolol in the treatment of hypertension.

1. A within-patient comparison showed that bethanidine, methyldopa and propranolol produced similar control of the blood pressure. 2. Unlike bethanidine, propranolol did not produce postural and exercise hypotension; methyldopa was intermediate in effect. 3. Overall side effects were of a similar incidence though there were differences in incidence of particular side effects.

Bethanidine↗
PubMedDate not supplied

Disposition of bethanidine, N-benzyl-N',N''-dimethylguanidine, in the rat, dog and man.

Bethanidine is metabolized in the rat and dog to a significant degree to N-benzyl-N'-methylguanidine, N-benzylguanidine, N-hydroxybenzyl-N'-methylguanidine, N-methylguanidine, N-hydroxybenzyl-N',N''-di-methylguanidine, and benzoic acid, whereas in man the drug is not metabolized. It is readily absorbed in all three species. The elimination kinetics in man show a difference between the urinary excretion rate and the rate of decline in the blood. Whole body autoradiograms showed a high concentration of drug in rat tissues rich in adrenergic nerve terminals, but insignificant penetration, if any, of the blood-brain barrier.

Adolescent↗
PubMed1975

Factors predisposing to postural hypotensive symptoms in the treatment of high blood pressure.

Symptoms due to orthostatic and exertional hypotension occurred in 23-4 per cent of 448 hypertensive patients treated with guanethidine, debrisoquine, or bethanidine. Symptoms were significantly more frequent in patients treated with guanethidine than in those treated with bethanidine or debrisoquine. Women rather than men and patients with radiological evidence of cardiomegaly, electrocardiographic evidence of left ventricular hypertrophy, or ST/T wave changes, developed these symptoms significantly more often than other patients. A raised blood urea was found more frequently in patients with postural hypotensive symptoms. Characteristically guanethidine produced early morning postural hypotensive symptoms, wheras hypotensive symptoms caused by bethanidine and debrisoquine occurred at other times of the day and particularly one to two hours after tablet ingestion. Debrisoquine and guanethidine had a significantly greater negative chronotropic effect than bethanidine. It is suggested that negative chronotropic effects of these drugs may potentiate hypotensive symptoms in patients with cardiovascular, renal, or cerebrovascular disease. It should be possible to minimize symptoms of postural hypotension by attention to predisposing factors and selection of treatment accordingly.

Bethanidine↗
PubMed1979

Possible role of brain norepinephrine in the hypothalamic hypophyseal adrenal system.

Intracisternal injection of bethanidine in rats decreased brain norepinephrine turnover without affecting its endogenous level, and increased both cardiac norepinephrine turnover and serum corticosterone level. A negative correlation was observed between brain norepinephrine turnover rate and serum corticosterone level. On the other hand, when cardiac norepinephrine turnover was suppressed by intraperitoneal injection of bethanidine, serum corticosterone did not change significantly. Next, ether inhalation was added after intracisternal injection of bethanidine. Then, serum corticosterone increased more even brain norepinephrine turnover was suppressed only slightly. These data may indicate that serum corticosterone increases by selective decrease in brain norepinephrine turnover via the humoral route; from the hypothalamus down to the adrenal cortex. Inversely, intracisternal injection of corticosterone increased brain norepinephrine turnover. These results suggest that brain norepinephrine may play an inhibitory role in the tonic regulation of CRF-ACTH secretion in the higher center than the hypothalamus and there may be a closed-loop feedback system between brain norepinephrine and serum corticosterone.

Animals↗
PubMed1977

New drugs in hypertension.

Clonidine, propranolol, bethanidine and debrisoquine effectively decrease blood pressure by suppressing renin secretion or interfering with function of the sympathetic nervous system. In man these compounds exert an antihypertensive effect within several hours or days and their duration of action is sufficient to permit administration twice or thrice daily. Clonidine and propranolol are especially useful if sexual dysfunction or postural hypotension is undesirable. Although bethanidine and debrisoquine may produce these adverse effects, they are beneficial in severe hypertension and produce fewer side effects than guanethidine. Clonidine frequently causes sedation, and rebound hypertension may occur with sudden cessation of therapy. Injudicious use of propranolol may provoke heart failure or asthma in susceptible individuals. The combination of a thiazide diuretic with propranolol and one of hydralazine, bethanidine and debrisoquine may be used to treat severe or complicated hypertension.

Antihypertensive Agents↗
PubMed1975

Sympathetic component of the pressor response to angiotensin II in the pithed rat after pretreatment with disulfiram.

Pressor responses to angiotensin II in the pithed rat were unaffected or slightly increased by procedures such as reserpine pretreatment, alpha and beta adrenoceptor blocking agents or bethanidine which inhibit the sympathetic system. Disulfiram-induced inhibition of angiotensin II pressor responses was unaffected by pretreatment with either alpha-adrenoceptor blockers or bethanidine. Pretreatment with disulfiram prevented infusions of angiotensin II from increasing the responses to spinal sympathetic outflow stimulation. After inhibition of pressor responses to angiotensin II by disulfiram the responses were restored by infusions of noradrenaline, or alpha-methyldopa. The restored responses, unlike control responses, were inhibited by phentolamine. The results suggest that angiotensin II facilitates neuronal release of noradrenaline and that this effect is revealed most clearly when post-synaptic angiotensin II receptors are blocked.

Adrenergic alpha-Antagonists↗
PubMed1978

The response of the circular muscle layer of the guinea-pig isolated vas deferens to transmural electrical stimulation.

1 Four preparations are described for the isolation of the response of the circular muscle of the guinea-pig vas deferens. These are the ;Furchgott' strip, the ;Vane' strip, the chain preparation and the perfused preparation.2 The four preparations were stimulated transmurally with pulses of supramaximal voltage. The threshold pulse width to which the strips and the perfused preparation responded was 0.025 ms and the maximum responses occurred at 0.1 ms. The threshold frequency was 2 Hz for strip and perfused preparations, the maxima being 20 or 50 Hz for strip preparations and 100 Hz for perfused preparations. The effect of varying the number of pulses per train was also investigated on the perfused vas. Responses occurred to train lengths of 8, 16, 32, 128 pulses, the maximum response being given at 128 pulses at 100 Hz; 256 pulses per train did not produce a further increase in response. The perfused preparation exhibited an after-response at certain frequencies and train lengths.3 Tetrodotoxin and the local anaesthetics, procaine and lignocaine, reversibly abolished the responses of strip and perfused preparations to transmural stimulation.4 The response to intramural nerve fibre stimulation was abolished by guanethidine or bethanidine; this abolition was reversed by dexamphetamine. Noradrenaline contracted strip preparations of circular muscle and raised the pressure in perfused preparations; noradrenaline was competitively antagonized by thymoxamine. The major part of the motor innervation of the circular layer seems to be noradrenergic.

Anesthetics, Local↗
PubMed1976

Angina in hypertensive patients. With particular reference to the negative chronotropic effects of sympatholytic therapy.

There was no significant difference in the blood pressure and heart rate response of hypertensive patients with and without angina to standardised exercise on a treadmill before and after anti-hypertensive treatment. There was no improvement in exercise tolerance in the hypertensive patients with angina treated with bethanidine, debrisoquine or guanethidine despite a reduction of resting and exercise heart rates after treatment. The negative chronotropic effect of these sympatholytic drugs was less than that of oxprenolol or propranolol, but the hypotensive response was greater. Both of these beta-receptor blocking drug produced an an improvement in exercise tolerance in patients with angina either alone or in combination with other hypotensive therapy. The best control of blood pressure and angina was often achieved by a combination of a sympatholytic drug and beta-receptor blocking drug. In hypertensive patients treated for several years, angina at presentation was occassionally reduced by reduction of blood pressure. Later onset of angina appeared to be unrelated to control of hypertension but to be due to coincidental coronary occlusion. There was no evidence that myocardial infarction was precipitated by postural or exercise hypotension although these effects occasionally precipitated angina.

Adrenergic beta-Antagonists↗
PubMed1976

Dihydroergotamine: an effective treatment for postural hypotension due to antihypertensive drugs (ganglion-blocking agents excepted).

In this study the effect of DHE on postural hypotension induced by major antihypertensive drugs was evaluated in 40 patients. 30 patients were treated with methyldopa, five with guanoxan sulphate and five with bethanidine sulphate. To obtain a more accurate picture of the effectiveness of DHE and to test the reproducibility of its effect, each patient was observed during five separate, successive periods: in the first period the antihypertensive agent was given alone; in the second period it was given along with placebo; in the third period it was given with DHE; in the fourth period the antihypertensive agent was given alone again; and in the fifth period it was again given with DHE. In the third and in the fifth period, DHE was administered at the same time as the antihypertensive agent in a dose of 9-15 mg/24 h (3-5 mg three times daily). The first dose was given 1 h before rising, and the daily dosage was progressively increased. The beneficial effect of DHE on postural hypotension was evaluated by assessing the clinical symptoms in a semiquantitative manner and by measuring the arterial blood pressure and heart rate in a recumbent and standing position. The results were classified as follows: excellent, good, moderate and no response. In most cases, DHE was found to be an effective drug for the treatment of postural hypotension, an improvement in clinical symptoms being noted in 57.5% of patients tested (excellent and good results). In these patients the standing arterial blood pressure showed a significant response (p less than 0.01). DHE did not interfere with the therapeutic effect of the antihypertensive agents. Furthermore, DHE did not affect the heart rate, nor did it give rise to any adverse reactions.

Adolescent↗