Beta-blocking drugs effects

Bailly D, Servant D, Blandin N, et al Effects of beta-blocking drugs in alcohol withdrawal a double-blind comparative study with propranolol and diazepam. Bio-med Pharmacother 46 419—424, 1992... 

Beta-blocking drugs given chronically lower blood pressure in patients with hypertension (see Chapter 11). The mechanisms involved are not fully understood but probably include suppression of renin release and effects in the central nervous system. These drugs do not usually cause hypotension in healthy individuals with normal blood pressure. 

Beta-blocking drugs (eg, propranolol) may be used as antianxiety agents in situations such as performance anxiety. The sympathetic nervous system overactivity associated with anxiety appears to be satisfactorily relieved by the fblockers, and a slight improvement in the nonsomatic components of anxiety may also occur. Adverse central nervous system effects of propranolol include lethargy, vivid dreams, and hallucinations. 

Gold MH, Holy AK, Roenigk HH Jr. Beta-blocking drugs and psoriasis. A review of cutaneous side effects and retrospective analysis of their effects on psoriasis. J Am Acad Dermatol 1988 19(5 Pt 1) 837-41. 

At this point one may put a question is hypotension a pvire vascular effect or does an other mechanism, humoral for instance, also contribute The fact that, after administration of a beta-blocking drug hypotension disappears, while only hypertension remains (Fig. 1), does not resolve the problem. In fact a hypothetic humoral mechanism may be inhibited by beta-blockers, similarly to other adrenergic metabolic effects. 

In rabbit klninogenolysis seems coupled with beta-receptor stimulation as it is inhibited by beta-blockers. In man the klninogenolysis, as other metabolic effects, such for instance as glycogenolysis, seems due to a sub-type of beta-receptor, in accordance with the slight inhibition obtainable with beta-blocking drugs. 

The / -adrenergic blocking agents block the lipolytic effects of catecholamines as well as those of TSH, ACTH and glucagon. In man the increased plasma FFA levels induced by catecholamine infusion are effectively inhibited by the beta blocking drugs butoxamide and propranolol. 

Adrenaline, noradrenaline Beta-adrenoceptor blocking drugs Potentiation of hypertensive effect. 

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. 

In the past, beta blockers were considered detrimental in patients with heart failure.60 As indicated in Chapter 20, these drugs decrease heart rate and myocardial contraction force by blocking the effects of epinephrine and norepinephrine on the heart. Common sense dictated that a decrease in myocardial contractility would be counterproductive in heart failure, and beta blockers were therefore contraindicated in heart failure.60,69 It is now recognized that beta blockers are actually beneficial in people with heart failure because these drugs attenuate the excessive sympathetic activity associated with this disease.56,64 As indicated earlier,... 

Beta blockers bind to beta-1 receptors on the myocardium and block the effects of norepinephrine and epinephrine (see Chapter 20). These drugs therefore normalize sympathetic stimulation of the heart and help reduce heart rate (negative chronotropic effect) and myocardial contraction force (negative inotropic effect). Beta blockers may also prevent angina by stabilizing cardiac workload, and they may prevent certain arrhythmias by stabilizing heart rate.40 These additional properties can be useful to patients with heart failure who also have other cardiac symptoms. 

Beta-blockers. There is some evidence that beta-adrenergic blocking drugs such as propranolol can cause bronchoconstriction in some patients. Some selectivity with beta2-adrenergic drugs can minimise this effect but caution should be exercised. 

Hydroxypropanolol (Fig. 4 [6b]) is an active metabolite that contributes to the beta blocking effect of propranolol. Its affinity (as the racemate) for the beta receptor in this instance was only 5% that of propranolol. If we assume that its enantioselectivity was similar to that of the parent drug, this would be equivalent to about 10% cross-reactivity for the / metabolite. It would appear that 4-hydroxypropanolol would contribute little to the apparent propranolol equivalents in plasma unless its concentration was markedly greater than that of the parent drug. 

Kostis JB, Rosen RC. Central nervous system effects of beta-adrenergic-blocking drugs the role of ancillary properties. Circulation 1987 75(1) 204-12. 

NSAIDs inhibited the effects of aU antihypertensive drug categories. However, in patients taking beta-block-ers and vasodilators, NSAIDs produced a greater increase in supine mean blood pressure than in patients taking diuretics, but only the pooled inhibitory effect of NSAIDs on the effects of beta-blockers achieved statistical significance. When the data were analysed by tjrpe of NS AID the meta-analysis showed that aU NSAIDs increased supine blood pressure, and that piroxicam, indometacin, and ibuprofen produced the most marked increases. However, only piroxicam had a statistically significant effect with respect to placebo. Aspirin,... 

Answer B. Propranolol is a nonselective blocker of beta adrenoceptors, whereas meto-prolol is Pj -selective. Metoprolol is less likely to block receptors in the bronchiolar smooth muscle and is less likely to cause bronchoconstriction, especially in asthmatic patients. Propranolol and metoprolol are considered to be equally effective as antiarrhythmics and in post-MI prophylaxis, and both are cardiodepressant. Drugs that appear to have both alpha- and beta-blocking actions include carvedilol and labetalol. 

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