Beta-adrenoceptor blockade

In one case, beta-adrenoceptor blockade masked an unexpected thyroid crisis, resulting in severe cerebral dysfunction before the diagnosis was made (184). 

VanDenMeiracker, A., Manln tVeld, A., Boomsma, F., Fischberg, D., Molinoff, P., and Schalekamp, M., Hemodynamic and beta-adrenergic receptor adaptations during long-term beta-adrenoceptor blockade. Studies with acebutolol, atenolol, pindolol, and propranolol in hypertensive patients, Circulation, Vol. 80, No. 4, 1989, pp. 903-914. 

It has been suggested that beta-blockers may predispose to obesity by reducing basal metabolic rate via beta-adrenoceptor blockade (197). Thermogenesis in response to heat and cold, meals, stress, and anxiety is also reduced by beta-adrenoceptor blockade, promoting weight gain (SEDA-16, 193). Betas-adrenoceptors have been implicated in this mechanism (198,199). Since propranolol blocks betas-receptors in vivo (200), it would be wise on theoretical grounds to avoid propranolol in obese patients nadolol is another non-selective beta-blocker that does not act on betas-adrenoceptors. 

Second-degree or third-degree heart block is a contraindication to beta-adrenoceptor blockade. If it is considered necessary for the control of dysrhythmias, a beta-blocker can be given after the institution of pacing. 

Pearson SB, Banks DC, Patrick JM. The effect of beta-adrenoceptor blockade on factors affecting exercise tolerance in normal man. Br J Clin Pharmacol 1979 8(2) 143-8. 

Kaiser P. Running performance as a function of the dose-response relationship to beta-adrenoceptor blockade. Int J Sports Med 1982 3(l) 29-32. 

Gordon NF. Effect of selective and nonselective beta-adrenoceptor blockade on thermoregulation during prolonged exercise in heat. Am J Cardiol 1985 55(10) D74-8. 

Walden RJ, Bhattacharjee P, Tomlinson B, Cashin J, Graham BR, Prichard BN. The effect of intrinsic sympathomimetic activity on beta-receptor responsiveness after beta-adrenoceptor blockade withdrawal. Br J Clin Pharmacol 1982 13(Suppl 2) S359-64. 

McDevitt DG. Beta-adrenoceptor blockade in hyperthyroidism. Shanks RG, editor. Advanced Medicine Topics in Therapeutics 3. London Pitman Medical 1977 100. 

Trap-Jensen J, Carlsen JE, Svendsen TL, Christensen NJ. Cardiovascmar and adrenergic effects of cigarette smokmg dming immediate non-selective and selective beta adrenoceptor blockade in hnmans. Em J Clin Invest 1979 9(3) 181-3. 

A single intravenous dose of labetalol 30 mg given to a woman with severe pregnancy-related hypertension 20 minutes before cesarean section was associated with significant neonatal beta-adrenoceptor blockade (hypoglycemia, bradycardia, and hypotension), and there were high labetalol concentrations in the umbilical cord blood (150-180 ng/ml) (13). 

Barrett, A.M. (1985) Cardiac beta-adrenoceptor blockade the quest for selectivity. Journal de Pharmacologic,... 

Frick, M. H. and Porsti, P. (1976) Combined alpha- and beta-adrenoceptor blockade with Labctatol in hypertension. Brit. med. J., 1, 1046. 

Weinstock, M., Weiss, C., and Gitter, S. (1977) Blockade of 5-HT receptors in the central nervous system by beta-adrenoceptor antagonists. Neuropharmacology, 16 273-276. 

Blomberg S, Rickstein SE (1988) Thoracic epidural anesthesia in conscious and anesthetized rats. Effects on central haemodynamics compared to cardiac beta adrenoceptor and ganglionic blockade. Acta Anaesthesiol Scand 32 166-172 Chemyakova IV, Zhukov VN, Osipov SA et at. (1994) Epidural and conduction anesthesia with azacaine in the experiment. Exp Clin Pharmacol 57 13-15 Defalque RJ, Stoelting VK (1966) Latency and duration of action of some local anesthetic mixtures. Anesth Analg 45 106-116... 

Neuroleptic drugs can reduce or block the pressor effects of alpha-adrenoceptor agonists. When using drugs with both alpha- and beta-adrenoceptor activity, neuroleptic drug blockade of alpha-adrenoceptors can lead to unopposed beta predominance, resulting in severe hypotension (622). 

Systemic Effects. Based on its pharmacologic activity, metipranolol theoretically shares with timolol and levobunolol the same potential for systemic beta-blockade. However, several studies show that the p-adrenoceptor blockade elicited by topical metipranolol may be less than that observed with timolol but more than that observed with betaxolol. 

Beta-blockade can result in sinus bradycardia, because blockade of sympathetic tone allows unopposed parasympathetic activity. Drugs with partial agonist activity may prevent bradycardia (52). However, heart rates under 60/ minute often worry the physician more than the patient in a retrospective study of nearly 7000 patients taking beta-adrenoceptor antagonists, apart from dizziness in patients with heart rates under 40/minute (0.4% of the total group), slow heart rates were well tolerated (53). 

Intermittent claudication has also been reported to be worsened by beta-adrenoceptor antagonists, but has been difficult to document because of the difficulty of study design in patients with advanced atherosclerosis. As early as 1975 it was reported from one small placebo-controlled study that propranolol did not exacerbate symptoms in patients with intermittent claudication (70). This has subsequently been supported by the results of several large placebo-controlled trials of beta-blockers in mild hypertension and reports of trials of the secondary prevention of myocardial infarction, in which intermittent claudication was not mentioned as an adverse effect, even though it was not a specific contraindication to inclusion (71). In addition, a comprehensive study of the effects of beta-adrenoceptor antagonists in patients with intermittent claudication did not show beta-blockade to be an independent risk factor for the disease (72). In men with chronic stable intermittent claudication, atenolol (50 mg bd) had no effect on walking distance or foot temperature (73). These findings have been confirmed in a recent meta-analysis of 11 randomized, controlled trials to determine whether beta-blockers exacerbate intermittent claudication (SEDA-17, 234). 

Presumably the beneficial effects of beta-blockade in this case were non-specific, since milrinone does not affect beta-adrenoceptors. 

More broadly, timolol therapy should be considered with caution in patients with any significant sign, symptom, or history for which systemic beta-blockade would be medically imwise.This includes disorders of cardiovascular or respiratory origin (e g., asthma, chronic bronchitis, and emphysema) as well as many other conditions. Spirometric evaluation after institution of timolol therapy may help to identify patients in whom bronchospasm develops after commencement of therapy. In general, however, patients with asthma and other obstructive pulmonary diseases should avoid this drug. Sympathetic stimulation may be essential to support the circulation in individuals with diminished myocardial contractility, and its inhibition by P-adrenoceptor antagonists may precipitate more severe cardiac feilure. 

O Shaughnessy KM, Fu B, Dickerson C, Thurston D, Brown MJ. 2000. The gain-of-function G389R variant of the betal-adrenoceptor does not influence blood pressure or heart rate response to beta-blockade in hypertensive subjects. Clin. Sci. 99 231-32... 

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