Propranolol-induced bronchoconstriction: A non-specific side-effect of β-adrenergic blocking therapy

Terpstra, G. K.; Raaijmakers, J. A. M.; Wassink, Guido

doi:10.1016/0014-2999(81)90154-0

Cited by 24 publications

(14 citation statements)

References 5 publications

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“…However, the effects of different β-blockers are not identical. The use of subtype nonselective β-blockers in early years has caused some major side effects including bronchial and blood vessel constriction [54,55] . This is largely due to the inhibition of β 2 AR in non-cardiac tissues such as the respiratory system and blood vessels.…”

Section: Carvedilol Paradoxmentioning

confidence: 99%

β-Adrenergic receptor subtype signaling in heart: From bench to bedside

2012

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β-Adrenergic receptor (βAR) stimulation by the sympathetic nervous system or circulating catecholamines is broadly involved in peripheral blood circulation, metabolic regulation, muscle contraction, and central neural activities. In the heart, acute βAR stimulation serves as the most powerful means to regulate cardiac output in response to a fight-or-flight situation, whereas chronic βAR stimulation plays an important role in physiological and pathological cardiac remodeling.There are three βAR subtypes, β 1 AR, β 2 AR and β 3 AR, in cardiac myocytes. Over the past two decades, we systematically investigated the molecular and cellular mechanisms underlying the different even opposite functional roles of β 1 AR and β 2 AR subtypes in regulating cardiac structure and function, with keen interest in the development of novel therapies based on our discoveries. We have made three major discoveries, including (1) dual coupling of β 2 AR to G s and G i proteins in cardiomyocytes, (2) cardioprotection by β 2 AR signaling in improving cardiac function and myocyte viability, and (3) PKA-independent, CaMKII-mediated β 1 AR apoptotic and maladaptive remodeling signaling in the heart. Based on these discoveries and salutary effects of β 1 AR blockade on patients with heart failure, we envision that activation of β 2 AR in combination with clinically used β 1 AR blockade should provide a safer and more effective therapy for the treatment of heart failure.

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Section: Carvedilol Paradoxmentioning

confidence: 99%

β-Adrenergic receptor subtype signaling in heart: From bench to bedside

2012

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“…Therefore, it is likely that the inhibitory effect of mexiletine on β 2 -adrenoceptor-mediated responses contributes to some extent to pharmacological actions of mexiletine at the therapeutic concentration range. Although β-adrenoceptor antagonists have little effect on pulmonary function in normal subjects, blockade of β-adrenoceptors can lead to life-threatening bronchoconstriction in asthmatic patients (Zaid and Beall 1966;Terpstra et al 1981). In asthmatic patients, circulating epinephrine may play an important role in the regulation of airway calibre by stimulating β 2 -adrenoceptors on airway smooth muscle or by reducing acetylcholine release from cholinergic nerves (Barnes 1995).…”

Section: Discussionmentioning

confidence: 98%

Mexiletine inhibits pharmacological actions of salbutamol through blockade of β 2 -adrenoceptors in bovine tracheal smooth muscle

Nakahara

Kubota

Sakamato

et al. 2001

Naunyn-Schmiedeberg's Archives of Pharmacology

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We examined the effects of mexiletine, a class Ib antiarrhythmic drug, on the changes in tension and adenosine 3',5'-cyclic monophosphate (cAMP) content induced by salbutamol and forskolin in bovine tracheal smooth muscle. Salbutamol (0.0001-1 microM) produced concentration-dependent relaxation in bovine tracheal smooth muscle contracted with methacholine (0.3 microM). Mexiletine (5-500 microM) caused the rightward shifts of concentration-response curves for the relaxant responses to salbutamol in a concentration-dependent manner. Mexiletine (5, 50 or 500 microM) did not change basal cAMP levels, whereas it concentration-dependently attenuated the salbutamol (0.1 microM)-induced cAMP accumulation. On the other hand, mexiletine (500 microM) did not change the concentration-response curves for the relaxant responses to forskolin (0.001-10 microM). Mexiletine slightly but significantly (P<0.05) increased forskolin (1 microM)-induced cAMP accumulation. In radioligand binding experiments, mexiletine concentration-dependently displaced the specific binding of [125I]cyanopindolol to beta-adrenoceptors on bovine tracheal smooth muscle membranes. By contrast, lidocaine, another class Ib antiarrhythmic drug, did not change the binding of [125I]cyanopindolol. These results demonstrate that mexiletine prevents the binding of beta2-adrenoceptor agonists to their receptors and thereby suppresses manifestation of subsequent pharmacological responses.

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“…Moreover, Terpstra, Raaijmakers & Wassink (1981) have pointed out that rat peritoneal mast-cells incubated with (+)-propranolol, as well as with the racemic form, release histamine. Our results rule out any dependence of 3-blocker potentiation upon a release of histamine because mepyramine did not affect (-)-propranolol potentiation of either LTC4…”

Section: Discussionmentioning

confidence: 99%

β₂‐Adrenoceptor blockade is the basis of guinea‐pig bronchial hyper‐responsiveness to leukotriene C₄ and other agonists

Bongrani

Folco

Razzetti

et al. 1983

British J Pharmacology

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1 Four P-adrenoceptor antagonists, namely (-)-propranolol, (+)-propranolol, ICI-118551 and (±)-practolol, were investigated for their effects on leukotriene C4 (LTC4)-induced bronchoconstriction in the anaesthetized guinea-pig. (-)-Propranolol was also investigated for its effects on acetylcholine and histamine bronchospasm in the anaesthetized guinea-pig, and on LTC4-induced contractions of guinea-pig isolated trachea and lung parenchyma. 2 The various 1-adrenoceptor antagonists potentiated, dose-dependently, the bronchoconstriction induced by threshold doses of LTC4 and the intensity of the potentiation correlated with the 12-blocking capacity possessed by the drugs.3 (-)-Propranolol potentiated the bronchospasm induced by threshold doses of acetylcholine and histamine but to a lesser degree than the LTC4-induced bronchospasm. 4 The airway hyper-responsiveness induced by (-)-propranolol was unaffected by pretreatment with mepyramine, cyproheptadine, phenoxybenzamine, atropine or indomethacin. 5 The airway hyper-responsiveness induced by (-)-propranolol persisted even in adrenalectomized or reserpine-treated guinea-pigs, although adrenalectomy induced some increase in airway responsiveness. 6 (-)-Propranolol had no effect on LTC4, histamine and acetylcholine-induced contractions of isolated trachea and lung parenchyma.7 The results show that the airway hyper-responsiveness induced by P-adrenoceptor antagonists generally correlates with their P2-blocking activity. The possibility remains that some other unknown mechanism(s) may also be implicated.

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Propranolol-induced bronchoconstriction: A non-specific side-effect of β-adrenergic blocking therapy

Cited by 24 publications

References 5 publications

β-Adrenergic receptor subtype signaling in heart: From bench to bedside

β-Adrenergic receptor subtype signaling in heart: From bench to bedside

Mexiletine inhibits pharmacological actions of salbutamol through blockade of β 2 -adrenoceptors in bovine tracheal smooth muscle

β₂‐Adrenoceptor blockade is the basis of guinea‐pig bronchial hyper‐responsiveness to leukotriene C₄ and other agonists

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Propranolol-induced bronchoconstriction: A non-specific side-effect of β-adrenergic blocking therapy

Cited by 24 publications

References 5 publications

β-Adrenergic receptor subtype signaling in heart: From bench to bedside

β-Adrenergic receptor subtype signaling in heart: From bench to bedside

Mexiletine inhibits pharmacological actions of salbutamol through blockade of β 2 -adrenoceptors in bovine tracheal smooth muscle

β2‐Adrenoceptor blockade is the basis of guinea‐pig bronchial hyper‐responsiveness to leukotriene C4 and other agonists

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β₂‐Adrenoceptor blockade is the basis of guinea‐pig bronchial hyper‐responsiveness to leukotriene C₄ and other agonists