A. BETA-ADRENOCEPTOR BLOCKING DRUGS (also see Table +lt;tab5-1+gt;). Mechanisms: Reduction

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A. BETA-ADRENOCEPTOR BLOCKING DRUGS (also see Table ). Mechanisms: * Reduction in cardiac output. Initially, this may be associated with a reflex increase in peripheral resistance. * With chronic therapy, there may be a decrease in peripheral resistance (the latter in part through a decrease in renin secretion and angiotensin production). Major indications for use in hypertension: * Mild and moderate hypertension; alone and in combination with vasodilators (to reduce reflex tachycardia and renin release). Other indications: * Angina pectoris , * Arrhythmias , glaucoma, migraine, familial tremor (see appropriate chapters for details) Contraindications and Warnings: * Cardiovascular: cardiac failure, sinus or AV node disease * Respiratory: airways disease, especially asthma. * Metabolic: diabetes is usually mentioned as a potential contraindica- tion although documented problems are difficult to find. (PgDn key for more text) Beta Blockers, Adverse Reactions: * Sedation, depression, lethargy, and sleep disturbances are common, especially when starting therapy. * Heart block, congestive failure, or bradyarrhythmias in patients with preexisting heart disease. These effects are dose-dependent and are major concerns in overdose toxicity. * Bronchospasm in patients with asthma or other airway disease * Treatment of overdosage requires special attention to maintaining car- diac output and rate. Isoproterenol, epinephrine, and glucagon have been used. Interactions: * Pharmacokinetic: Because of the significant first pass effect, drugs that decrease liver blood flow (including beta-blockers themselves) will increase bioavailability and circulating levels of most beta-blockers. * Pharmacodynamic: Severe hypertension may result from administration of epinephrine when B-receptors are blocked. (Home to return to top of file)


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