(Original placard by Jaanu)
Can someone please make plain this to me? Thanks in advance
Why does an alpha receptor antagonist drug reduce hypertension but cause reflected tachycardia?
And why is a beta 2 receptor agonist used conducive to the treatment of asthma?
All adrenergic (alpha and beta) receptors are G-protein-coupled receptors, and are located in multiform tissues. Alpha1 receptors are located attached smooth muscle tissue in walls of veins, and on the subject of activation through Gq and IP3 during the time that the second messenger, release intracellular Ca2+, causing allay muscle contraction. This causes the lumen of the veins to compress, increasing blood pressure. Therefore, if you gave ~y alpha1 receptor antagonist, e.g. doxazosin, it would source hypotension. This reduction in blood oppression is sensed by the cardiorespiratory middle in the medulla oblongata, which causes activation of the tender nervous system, sending more action potentials into disgrace towards the sinoatrial node in the purpose, causing the heart to beat faster (tachycardia). This is a reflective in order to increase blood embarrassment.
Bear in mind not to derange alpha1 and alpha2 receptors, as they be under the necessity opposite effects with regards to vital fluid pressure (alpha2 receptor agonists, e.g. clonidine, will reduce blood pressure).
Some beta2 receptors are located forward the smooth muscle cells of bronchioles in the lungs. Upon activation through Gs, intracellular cAMP concentration is increased. cAMP inhibits some enzyme called myosin light chain kinase, and activates one enzyme called myosin light chain phosphatase. Both of these actions causes allay muscle relaxation, causing bronchodilation, which relieves symptoms of an asthma attack, e.g. shortness of respired air. Therefore, beta2 receptor agonists, e.g. salbutamol (straight-acting) and salmeterol (long-acting) be able to be used in an acute asthma criticise and in asthma maintenance therapy, respectively.
Hope this helps!
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