Antiadrenergics

Antiadrenergics are drugs capable of lowering transmitter output from sympathetic neurons, i.e sympathetic tone . Their action is hypotensive (indication hypertension, p. 312) however, being poorly tolerated, they enjoy only limited therapeutic use. 

Side effects. Lassitude, dry mouth rebound hypertension after abrupt cessation of clonidine therapy. 

Methyldopa (dopa = dihydroxy-phenylalanine), as an amino acid, is transported across the blood-brain barrier, decarboxylated in the brain to a-methyldopamine, and then hydroxylat-ed to a-methyl-NE The decarboxylation of methyldopa competes for a portion of the available enzymatic activity, so that the rate of conversion of L-dopa to NE (via dopamine) is decreased. The false transmitter a-methyl-NE can be stored however, unlike the endogenous mediator, it has a higher affinity for a2- than for ai-receptors and therefore produces effects similar to those of clonidine. The same events take place in peripheral adrenergic neurons. 

Adverse effects. Fatigue, orthostatic hypotension, extrapyramidal Parkin-son-like symptoms (p. 88), cutaneous reactions, hepatic damage, immune-hemolytic anemia 

Reserpine, an alkaloid from the Rauwolfia plant, abolishes the vesicular storage of biogenic amines (NE, dopamine = DA, serotonin = 5-HT) by inhibiting an ATPase required for the vesicular amine pump. The amount of NE re-Liillmann, Color Atlas of Pharmacology 2000 Thieme All rights reserved. Usage subject to terms and conditions of license. 

Reserpine, an alkaloid from the climbing shrub Rauwolfm serpentina (native to the Luellmann, Color Atlas of Pharmacology All rights reserved. Usage subject to terms 

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Venlafaxine (48) is a stmcturaHy novel phenylethylamine derivative that strongly inhibits both noradrenaline and serotonin reuptake. It lacks anticholinergic, antihistaminergic, and antiadrenergic side effects. As compared to placebo, most common adverse events are nausea, somnolence, dizziness, dry mouth, and sweating. Venlafaxine-treated patients also experienced more headaches and nausea, but less dry mouth, dizziness, and tremor than patients treated with comparator antidepressants. 

A special feature of the iris is its autonomic innervation. Sympathetic activation widens the aperture of the iris whereas impulses from the parasympa thetic nervous system decrease the aperture size. Therefore adrenergic agonists and anticholinergic compounds both increase the aperture of the iris, i.e., cause mydriasis, and antiadrenergic and cholinergic agonists decrease it, i.e., cause miosis. The iris can thus be considered an excellent mirror reflecting the balance of the autonomic nervous system in the body. " ... 

The role of the aromatic ring in the alkoxy- and alkylbenzenes which follow is not nearly as well defined as it is with the adrenergic and antiadrenergic drugs. 

Further class IA drugs include the open state blockers procainamide and disopyramide with electrophysiolog-ical effects similar to those of quinidine procainamide lacks the antimuscarinic and antiadrenergic effects. Characteristic side effects of procainamide are hypotension and immunological disorders. 

Antiadrenergic drugs—drug that block adrenergic nerve fibers. These dm i block the adrenergic nerve fibers within the central nervous system (CNS) or within the peripheral nervous system. 

Antiadrenergic drag s are used mainly for the treatment of certain cardiac arrhythmias and hypertension (see the Summary Drug Table Adrenergic Blocking Dmgp). 

Some of the adverse reactions associated with the administration of centrally acting antiadrenergic dragp include dry mouth, drowsiness, sedation, anorexia, rash, malaise and weakness. Adverse reactions associated with the administration of the peripherally acting antiadrenergic dragp include hypotension, weakness, light-headedness, and bradycardia... 

The peripherally acting antiadrenergic drugs are contraindicated in patients with a hypersensitivity to any of the drugs. Reserpine is contraindicated in patients who have an active peptic ulcer or ulcerative colitis and in... 

Antiadrenergic drags (centrally acting)—for example, guanabenz (Wytensin) and guanfacine (Tenex)... 

Antiadrenergic dragp (peripherally acting)—for example, guanadrel (Hylorel) and guanethidine (Ismelin)... 

Type II drugs include /Tadrenergic antagonists clinically relevant mechanisms result from their antiadrenergic actions. /3- Blockers are most useful in tachycardias in which nodal tissues are abnormally automatic or are a portion of a reentrant loop. These agents are also helpful in slowing ventricular response in atrial tachycardias (e.g., AF) by their effects on the AV node. 

The following therapeutic measures should be instituted promptly (1) suppression of thyroid hormone formation and secretion (2) antiadrenergic therapy (3) administration of corticosteroids and (4) treatment of associated complications or coexisting factors that may have precipitated the storm (Table 20-2). 

Antiadrenergic therapy with the short-acting agent esmolol is preferred because it can be used in patients with pulmonary disease or at risk for cardiac failure and because its effects can be rapidly reversed. 

Antiadrenergics and atypical antipsychotics can be used as augmenting agents. 

Antiadrenergic drugs (prazosin) can be useful in some patients with PTSD, and antipsychotics (risperidone, quetiapine, and olanzapine) may be used as augmenting agents in partial responders. 

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