Sympathetic nervous system beta blockers

Beta-biockers/Other sympathetic nervous system suppressants - When beginning therapy, the -blocker dosage should be equal to 80 to 160 mg/day propranolol in divided doses. If -blockers are contraindicated, use methyidopa 250 to 750 mg twice daily give for at least 24 hours before starting minoxidil due to delay in onset. Clonidine may also be used to prevent tachycardia induced by minoxidil usual dosage is 0.1 to 0.2 mg twice daily. 

Must be used in conjunction with diuretic (except dialysis patients) and beta-blocker or other sympathetic nervous system depressant (to prevent reflex tachycardia)... 

Drugs that block beta-1 receptors on the myocardium are one of the mainstays in arrhythmia treatment. Beta blockers are effective because they decrease the excitatory effects of the sympathetic nervous system and related catecholamines (norepinephrine and epinephrine) on the heart.5,28 This effect typically decreases cardiac automaticity and prolongs the effective refractory period, thus slowing heart rate.5 Beta blockers also slow down conduction through the myocardium, and are especially useful in controlling function of the atrioventricular node.21 Hence, these drugs are most effective in treating atrial tachycardias such as atrial fibrillation.23 Some ventricular arrhythmias may also respond to treatment with beta blockers. 

Beta-adrenoceptor blockers. The realisation that the coiuse of chronic heart failure can be adversely affected by activation of the renin-angiotensin-aldosterone and sympathetic nervous systems led to exploration of possible benefit from P-adrenoceptors in a condition where, paradoxically, such drugs can have an adverse effect. Clinical trials have, indeed, shown that bisoprolol, carvedilol or metoprolol lower mortality and decrease hospitalisation when added to diuretics, digoxin and an ACE inhibitor (see below). 

The adrenergic responses to hypoglycemia (the warning signals ) are mediated by the sympathetic nervous system (e.g., tachycardia, restlessness). Beta blockade masks these symptoms, so that a decrease in blood sugar may go unnoticed by the patient. Long-term therapy with beta-blockers may also lead to insulin resistance. 

Non-selective beta blockers such as propranolol also block the beta2 receptors in the bronchi so that the normal bronchodilation, which is under the control of the sympathetic nervous system, is reduced or abolished. As a result the bronchoconstriction of asthma can be made worse. Cardioselective beta blockers on the other hand, preferentially block betaj receptors in the heart, with less effect on the beta2 receptors, so that beta2 stimulating bronchodilators, such as isoprenaline, salbutamol and terbutaline, continue to have bronchodilator effects. 

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