This site is intended for healthcare professionals
Login | Register (NOW FREE)

Medical search

beta 2 adrenoceptor antagonists

FREE subscriptions for doctors and students... click here
You have 3 open access pages.

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

Reference:

Links:

The information provided herein should not be used for diagnosis or treatment of any medical condition. A licensed medical practitioner should be consulted for diagnosis and treatment of any and all medical conditions. Copyright 2016 Oxbridge Solutions LtdĀ®. Any distribution or duplication of the information contained herein is strictly prohibited. Oxbridge Solutions LtdĀ® receives funding from advertising but maintains editorial independence. GPnotebook stores small data files on your computer called cookies so that we can recognise you and provide you with the best service. If you do not want to receive cookies please do not use GPnotebook.