Antagonism of adrenergic neuron blockade in hypertensive subjects

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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“…This observation would be consistent with two studies that failed to show guanethidine antagonism following a single dose of TCA (100,101).…”

Section: Drug Interactions With Tricyclic Antidepressantssupporting

confidence: 85%

A Review of the Cardiovascular Effects and Toxicity of Tricyclic Antidepressants

Jefferson

1975

Psychosomatic Medicine

227

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“…Clinical observations also indicate that amphetamine and related drugs specifically antagonize the hypotensive action of bretylium and guanethidine (Gulati, Dave, Gokhale & Shah, 1966). In the present experiments methylamphetamine could reverse the block by xylocholine, bretylium or guanethidine of the responses to stimulation of the postganglionic sympathetic nerve.…”

Section: Discussionsupporting

confidence: 51%

Cholinergic Link Hypothesis and Sympathetic Transmission at the Nictitating Membrane of the Dog

Arya

Gulati

1968

British Journal of Pharmacology and Chemotherapy

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“…For example, it has been reported that s-adrenergic blocking agents can protect a-adrenergic receptors against POB blockade (Olivares et ~., 1967;Patil et ~., 1968), and this effect has been attributed to a competition between a-and s-adrenergic blocking agents for receptor sites (Gulati et ~., 1965). The finding that hypothermia (15 0 C) abolished s-adrenergic reactivity of the cardiovascular system in the dog and rat, while a-adrenergic reactivity was maintained, is also consistent with the above concept (Price et~., 1967).…”

Section: \mentioning

confidence: 99%

Transformation of Adrenergic Receptors in the Myocardium

1973

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·ABSTRACTThe present series of experiments provided evidence that the generally accepted distinction between a-and s-adrenergic receptors is not immutable. In frog hearts and rat atria 3H-phenoxybenzamine (3H-POB ) blocked inotropic responses to catecholamines only at temperatures below l7 0 C and potentiated responses ab ove 23 0 C, and considerably more radioactivity was bound to the myocardium at lower temperatures. The converse was true for l4C-propranolol, and the potency of a-and s-adrenergic agonists was shawn to parallel the effectiveness of the blocking agents. Alkylation of a-adrenergic receptors by POB at l4 0 c prevented the appearance of s-adrenergic receptors when the temperature was subsequently raised ta 24 o C.Phentolamine prevented block by 3H-POB and considerably reduced its binding ta the myocardium at low but not at high temperatures. After exposure ta unlabelled POB in the presence of phentolamine at low temperature and thorough washing, exposure to 3H-POB produced a IIpositive label" of the adrenergic receptors, which was localized in a 20,000 9 (ll mitochondrial ll ) and in a IIsoluble protein" fraction. Pretreatment of rats with 6-hydroxydopamine, but not with reserpine, prevented the appearance of oe-adrenergic receptor charac.teristics in left atria at low temperatures; this indicated that adrenergic innervation, but probably not stores of neurotransmitter, is necessary to allow transformation of the receptors. It is suggested that a-and S-adrenergic receptors may be different allosteric conformations of the same molecule.

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Antagonism of adrenergic neuron blockade in hypertensive subjects

Abstract: The effects of dextroamphetamine, methamphetamine, methylphenidate, nialamide, imipramine, and ephedrine

Cited by 40 publications

References 3 publications

A Review of the Cardiovascular Effects and Toxicity of Tricyclic Antidepressants

A Review of the Cardiovascular Effects and Toxicity of Tricyclic Antidepressants

Cholinergic Link Hypothesis and Sympathetic Transmission at the Nictitating Membrane of the Dog

Transformation of Adrenergic Receptors in the Myocardium

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