Guanethidine antidepressants

The amphetamines and the anorexiants should not be given during or within 14 days after administration of monoamine oxidase inhibitors (see Chap. 31) because the patient may experience hypertensive crisis and intracranial hemorrhage. When guanethidine is administered with the amphetamines or the anorexiants, the antihypertensive effect of guanethidine may decrease. Coadministration of the amphetamines or the anorexiants with the tricyclic antidepressants may decrease the effects of the amphetamines or the anorexiants. 

Drugs that may affect nasal decongestants include beta blockers, furazolidone, guanethidine, methyidopa, MAO inhibitors, rauwolfia alkaloids, tricyclic antidepressants, urinary acidifiers, and urinary alkalinizers. 

Drugs that may affect methylphenidate include MAOIs. Drugs that may be affected by methylphenidate hydrochloride include guanethidine, anticonvulsants (eg, phenytoin, phenobarbital, primidone), selective serotonin reuptake inhibitors, coumarin anticoagulants, and tricyclic antidepressants. 

The tricyclic antidepressants (e.g., desipramine and amitriptyline) and some phenothiazines block the sympathetic neuronal amine uptake system they thereby would also block the uptake of guanethidine and thus reduce its hypotensive effectiveness. Conversely, guanethidine competitively inhibits the uptake of drugs that are substrates for neuronal uptake, such as the indirectly acting adrenomimetics, or sympathomimetics (see Chapter 10). 

Can antidepressants such as tricyclics or buproprion augment the effect of stimulants on nondepressed children with ADHD Randomized controlled trials have yet to address this question. Nonetheless, such combinations are common in clinical practice. One case report showed leukopenia in a child treated with a combination of MPH and tricyclics for 4 months, although the doses were not specified (Burke et ah, 1995). Another case report indicated that obsessive-compulsive symptoms developed secondary to the combination of MPH and tricyclics (Pataki et ah, 1993). On a cautionary note, MPH has been found to interact with guanethidine to produce paradoxical hypotension. Patients on monoamine oxidose (MAO) inhibitors are likely to develop hypertensive crises if given a stimulant. 

Tricyclic antidepressants potentiate the pressor effects of directly acting sympathomimetic amines, such as adrenaline (epinephrine) or noradrenaline (norepinephrine), to cause hypertension. Small amounts of these, such as may be present in local anaesthetic solutions, can be dangerous. Tricyclic antidepressants will inhibit the antihypertensive effects of the older anti hypertensive drugs, such as adrenergic neurone-blocking agents, e.g. guanethidine, a-methyl-DOPA, and clonidine. 

Because neuronal uptake is necessary for the hypotensive activity of guanethidine, drugs that block the catecholamine uptake process or displace amines from the nerve terminal (see Chapter 6) block its effects. These include cocaine, amphetamine, tricyclic antidepressants, phenothiazines, and phenoxybenzamine. 

Release can be blocked by drugs such as guanethidine and bretylium. After release, norepinephrine diffuses out of the cleft or is transported into the cytoplasm of the terminal (uptake 1 [1], blocked by cocaine, tricyclic antidepressants) or into the postjunctional cell (uptake 2 [2]). Regulatory receptors are present on the presynaptic terminal. (SNAPs, synaptosome-associated proteins VAMPs, vesicle-associated membrane proteins.)... 

Patients taking certain systemic medications are also more sensitive to the pressor effects of phenylephrine. In individuals taking atropine, the pressor effect of phenylephrine is augmented, and tachycardia can occur. Tricyclic antidepressants and monoamine oxidase (MAO) inhibitors also potentiate the cardiovascular effects of topical phenylephrine. The concomitant use of phenylephrine is contraindicated with these agents, even up to 21 days after cessation of MAO inhibitor therapy. Similarly, patients taking reserpine, guanethidine, or methyldopa are at increased risk for adverse pressor effects from topical phenylephrine because of denervation hypersensitivity accompanying the chemical sympathectomy. 

The drug is contraindicated in patients taking MAO inhibitors, tricyclic antidepressants, reserpine, guanethidine, or methyldopa. 

Interactions of sympathomimetics with other vasoactive drugs are complex. Some drugs block the reuptake mechanism for noradrenaline in adrenergic nerve terminals and potentiate the pressor effects of noradrenaline e.g. cocaine, tricyclic antidepressants or highly noradrenaline-selective reuptake inhibitors such as roboxetine. Others deplete or destroy the intracellular stores within adrenergic nerve terminals (e.g. reserpine and guanethidine) and thus block the action of indirect S5unpathomimetics. 

Patients taking monoamine oxidase inhibitors, anticholinergic drugs (such as tricyclic antidepressants), propranolol, reserpine, guanethidine, and methyldopa should be monitored closely if phenylephrine is used (SEDA-16, 542) (16). 

Tricyclic antidepressants reverse the hypotensive effects of postganglionic blocking agents, guanethidine, reser-pine, clonidine, and alpha-methyldopa, and the addition of a tricyclic can result in loss of blood pressure control (159,179). Sudden withdrawal of a tricyclic compound from a patient stabilized with these compounds can also result in serious hypotension. An additional reason for avoiding drugs such as reserpine, methyldopa, and... 

Clinically important, potentially hazardous interactions with antihypertensives, dexamethasone, ephedra, furazolidone, guanethidine, guarana, MAO inhibitors, methyldopa, oxprenolol, phenelzine, phenylpropanolamine, selegiline, tranylcypromine, tricyclic antidepressants... 

The antihypertensive effects of guanethidine may be partially or totally reversed by the mixed-acting sympathomi-metics. Halogenated hydrocarbon anesthetics may sensitize the myocardium to the effects of catecholamines. Use of vasopressors may lead to serious arrhythmias. MAO inhibitors, such as tranylcypromine, increase the pressor response to mixed-acting vasopressors. Possible hypertensive crisis and intracranial hemorrhage may occur. This interaction may also occur with furazolidone, an antimicrobial with MAO inhibitor activity. In obstetrics, if vasopressor drugs are used either to correct hypotension or are added to the local anesthetic solution, some oxytocics may cause severe persistent hypertension in the presence of mephenteramine. The pressor response of mephenteramine may be attenuated by tricyclic antidepressants, which block the uptake of norepinephrine. 

Drug interactions tricyclic antidepressants block reuptake and the action of guanethidine ttj blockers... 

---