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beta 2 adrenoceptor antagonists

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Beta-blockers reduce the effects of the sympathetic nervous system on the cardiovascular system.

The blockade of beta-1 adrenoreceptors is negatively chronotropic and inotropic, and delays conduction through the AV node. If beta-2 receptors are blocked then this leads to coronary and peripheral vasoconstriction. Thus drugs which are relatively specific for beta-1 receptors, "cardioselective", have been developed e.g. atenolol and metoprolol.

  • there are 3 types of beta receptors
    • beta 1-Adrenoceptors
      • situated in the cardiac sarcolemma
        • if activated, they lead to an increase in the rate and force of myocardial contraction (positive inotropic effect) by opening the calcium channels
    • beta 2-Adrenoceptors
      • found mainly in bronchial and vascular smooth muscles
        • if activated, they cause broncho- and vaso-dilatation
          • there are, however, sizable populations of beta 2-Adrenoceptors in the myocardium, of about 20%-25%, which leads to the cardiac effects of any beta2-Adrenoceptors stimulation. There is a relative up-regulation of these receptors to about 50% in heart failure
    • beta 3 Adrenoceptors
      • the role of beta 3-Adrenoceptors in the heart is not yet fully identified and accepted

  • beta-blockers are classified into three generations
    • the first generation agents (such as Propranolol, Sotalol, Timolol, and Nadolol), are nonselective and block beta 1 and beta 2 receptors
      • blocking beta1-receptors affects the heart rate, conduction and contractility, while blocking beta 2-receptors, tends to cause smooth muscle contraction, therefore, bronchospasm in predisposed individuals

    • second-generation agents or the cardioselective agents (such as Atenolol, Bisoprolol, Celiprolol, and Metoprolol)
      • block beta 1-receptors in low doses but are capable of blocking beta 2-receptors in higher doses
        • selective mode of action makes the use of these agents more suitable in patients with chronic lung disease or those with insulin-requiring diabetes mellitus
        • there is evidence that, in patients with COPD, cardioselective beta blockers do not change FEV1 or increase respiratory symptoms
        • there is evidence that cardioselective beta blockers are >20 times more selective for ß1 than ß2 receptors and should carry less risk of bronchoconstriction in reactive airways disease
        • cardioselectivity varies between agents with the Bisoprolol among the most selective

    • third generation agents have vasodilatory properties
      • action is either selective (Nebivolol) or nonselective (Carvidolol and Labetolol)
      • vasodilatory properties are mediated either by nitric oxide release as for Nebivolol or Carvidolol or by added alpha-adrenergic blockade as in Labetolol and Carvidolol
      • a third vasodilatory mechanism, as in Pindolol and Acebutolol, acts via beta 2-intrinsic sympathomimetic activity (ISA)
      • these beta-blockers therefore have the capacity to stimulate as well as to block adrenergic receptors and tend to cause less bradycardia than the other beta-blockers and may cause less coldness of the extremities



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