Insidious and Prolonged Antagonism of Guanethidine by Amitriptyline

Meyer, Jerry F.

doi:10.1001/jama.1970.03170350053016

Cited by 29 publications

(5 citation statements)

References 4 publications

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“…Once TCA are stopped the antihypertensive action of guanethidine returns slowly over a period of days (averaging about 5, although a delay of 18 days has been reported) (98). After doxepin is discontinued an initial rebound hypertensive response occurs, which is similar to that occurring when chlorpromazine is discontinued, but which has not been noted with the other tricyclics.…”

Section: Drug Interactions With Tricyclic Antidepressantsmentioning

confidence: 98%

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A Review of the Cardiovascular Effects and Toxicity of Tricyclic Antidepressants

Jefferson

1975

Psychosomatic Medicine

227

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The tricyclic antidepressants have potent and complex effects on the cardiovascular system, both directly and through interactions with other drugs. Through a combination of anticholinergic activity, direct myocardial depressant activity and an effect on the adrenergic neuron, they can cause a combination of arrhythmias, blood pressure abnormalities and congestive heart failure. These changes, although most common with overdose, can occur at therapeutic levels. In addition a number of drug-drug interactions can occur between the tricyclics and agents used in the treatment of cardiovascular disease, as exemplified by tricyclic antagonism of the antihypertensive effect of guanethidine. Awareness of these factors is necessary to insure proper therapeutic utilization of the tricyclics as well as to treat effectively their toxicity.

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Section: Drug Interactions With Tricyclic Antidepressantsmentioning

confidence: 98%

“…A patient whose pressure was controlled on 75 mg of guanethidine prior to the start of amitriptyline (25 mg t.i.d.) eventually required 300 mg of guanethidine for adequate pressure control (98). At least one death has been related to this interaction (99).…”

Section: Drug Interactions With Tricyclic Antidepressantsmentioning

confidence: 99%

A Review of the Cardiovascular Effects and Toxicity of Tricyclic Antidepressants

Jefferson

1975

Psychosomatic Medicine

227

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“…Effects on blood pressure Theoretically, TCAs can raise blood pressure by potentiating the pressor effects of catecholamines due to their blocking effect on noradrenaline uptake in adrenergic neurones. Although low doses of imipramine have been shown to raise blood pressure in animals, reports in man on this subject are few and mostly deal with the interaction between the TCAs and the adrenergic-neurone-blocking antihypertensive drugs such as guanethidine and clonidine (Meyer et al, 1970;Briant et al, 1973).…”

Section: Tricycic Antidepressant Drugsmentioning

confidence: 99%

Cardiac effects of antidepressant drugs. A comparison of the tricyclic antidepressants and fluvoxamine.

Roos¹

1983

Brit J Clinical Pharma

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1 The cardiovascular effects of the tricyclic antidepressants (TCAs) are reviewed and compared with those of fluvoxamine, a new 5-hydroxytryptamine (5-HT) re-uptake inhibitor. 2 The TCAs have important effects on the heart, related to their anticholinergic and quinidine-like properties. The major side effects in therapeutic dosage include heart rate increase, postural hypotension and slight prolongation of the intraventricular conduction time and QT interval. In toxic dosage (or normal dosage in patients with severe heart disease) both advanced heart block and ventricular arrhythmias can occur, together with clinically important loss of myocardial contractile force. 3 Fluvoxamine has no effects on the heart except for a statistically (but not clinically) significant slowing of the heart rate.

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“…TADs have also been found to block the antihypertensive action of the adrenergic neurone blocking agents, guanethidine, bethanidine and debrisoquine (Skinner et al, 1969;Meyer et al, 1970); and also to interfere with the antihypertensive action of clonidine (Briant et al, 1973). It is thought by some that they are also contraindicated when patients are receiving methyldopa (White, 1965).…”

Section: Introductionmentioning

confidence: 99%

Cardiovascular responses to mianserin hydrochloride: a comparison with tricyclic antidepressant drugs.

Burgess,

Turner,

Wadsworth

1978

Brit J Clinical Pharma

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1. The cardiovascular responses of mianserin hydrochloride and tricyclic antidepressant drugs were investigated using non‐invasive methods of cardiac investigation. A study of the interaction of mianserin and antihypertensive drug therapy is reported. 2. In six normal volunteers, mianserin hydrochloride 20 mg was shown to prolong the corrected Q‐T interval at 150 min (P less than 0.001). It did not affect heart rate, systolic time intervals or the peak normalized derivative of the apexcardiogram. Amitriptyline 50 mg increased the corrected pre‐ejection period interval (PEPI) and the PEP/left ventricular ejection time (LVET) ratio of the systolic time intervals at 150 min (P less than 0.001). Q‐T interval was shortened at 90 minutes. 3. In a double‐blind patient study, clomipramine increased heart rate, P‐R interval, QRS and corrected Q‐T interval in one patient at 2 weeks. Mianserin prolonged corrected Q‐T interval at 1 week but this returned to the pretreatment time by 2 weeks in two patients. 4. In an open study, mianserin 20 mg three times daily did not antagonize the hypotensive action of propranolol or propranolol and hydrallazine in three patients. 5. In a double‐blind study in three patients with desmethylimipramine 25 mg three times daily, mianserin 20 mg three times daily did not antagonize the hypotensive action of either guanethidine or bethanidine.

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Insidious and Prolonged Antagonism of Guanethidine by Amitriptyline

Cited by 29 publications

References 4 publications

A Review of the Cardiovascular Effects and Toxicity of Tricyclic Antidepressants

A Review of the Cardiovascular Effects and Toxicity of Tricyclic Antidepressants

Cardiac effects of antidepressant drugs. A comparison of the tricyclic antidepressants and fluvoxamine.

Cardiovascular responses to mianserin hydrochloride: a comparison with tricyclic antidepressant drugs.

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