Beta-adrenergic agents

Anticholinergics, like atropine and its derivative ipratropium bromide block cholinergic pathways that cause airway constriction. They may provide added bronchodi-lator effect in patients who are receiving beta -adrenergic agents for asthma. 

Dailey MO, Schreru s J, Schuhnan H (1988) Hormone receptors on cloned T lymphocytes, hr creased responsiveness to liistamirie, prostaglandins, and beta-adrenergic agents as a late stage event in T cell acdvadori. J Immunol 140 2931—2936. 

Mansfield LE, Nelson HS. Effect of beta-adrenergic agents on immunoglobulin G levels of asthmatic subjects. Int Arch Allergy Appl Immunol 1982 68(1) 13-16. 

Treat seizures (see p 22), arrhythmias (pp 12-15), and hypotension (p 16) if they occur. Tachyarrhythmias and hypotension are best treated with a beta-adrenergic agent (see B, below). 

We have reported on the effect of increasing vehicle viscosity on the ocular bioavailability of the beta-adrenergic agent L-653,328 (Grove et al, 1990). It has been suggested that since L-653,328 is a prodrug the vehicle could exert an influence on the corneal esterases. We have therefore examined the effects of vehicle on another B1-antagonist, betaxolol, that is not metabolised in the cornea and have also compared the bioavailability with commercially available formulations. 

D. J. Smith, The pharmacokinetics, metabolism, and tissue residues of beta-adrenergic agents in livestock, J. Anim. Sci., 1998, 76, 173-194. 

Hydralazine is usually used in combination with other drugs. In recent years, it has been found to be especially useful when used with beta-adrenergic blocking agents and diuretics (3,4). 

Drugs that may affect nateglinide include nonsteroidal anti-inflammatory agents (NSAIDs), salicylates, monoamine oxidase inhibitors, rifamycins, MAOIs, and nonselective beta-adrenergic blocking agents, thiazides, corticosteroids, thyroid products, and sympathomimetics. 

Mechanism of action - Disopyramide is a class lA antiarrhythmic agent that decreases the rate of diastolic depolarization (phase 4), decreases the upstroke velocity (phase 0), increases the action potential duration of normal cardiac cells, and prolongs the refractory period (phases 2 and 3). It also decreases the disparity in refractoriness between infarcted and adjacent normally perfused myocardium and does not affect alpha- or beta-adrenergic receptors. 

Nonallergic bronchospasm (eg, chronic bronchitis, emphysema) n general, these patients should not receive propafenone or other agents with beta-adrenergic blocking activity. 

Drugs that may interact with clonidine include beta-adrenergic blocking agents and tricyclic antidepressants. 

Pharmacology These agents are synthetic adrenocortical steroids with basic glucocorticoid actions and effects. Glucocorticoids may decrease number and activity of inflammatory cells, enhance effect of beta-adrenergic drugs on cyclic AMP production, inhibit bronchoconstrictor mechanisms, or produce direct smooth muscle relaxation. Inhaler use provides effective local steroid activity with minimal systemic effect. 

Thyroid Beta-adrenergic blocking agents may mask clinical signs of hyperthyroidism (eg, tachycardia). 

Mechanism of Action An antihypertensive and antiglaucoma agent that blocks beta,-adrenergic receptors in cardiac tissue. Reduces aqueous humor production. Therapeutic Effect Slows sinus heart rate, decreases BP, and reduces intraocular pressure (lOP). 

Mechanism of Action Adirect-acting inotropic agent acting primarily on beta,-adrenergic receptors. Therapeutic Effect Decreases preload and afterload, and enhances myocardial contractility, stroke volume, and cardiac output. Improves renal blood flow and urine output. 

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