Alex is seemingly due to contraction agonists from

Alex BivinsMr. HsuAP BiologyJanuary 30, 2018Albuterol Pathways Albuterol is a common drug referred to as a bronchodilator that relaxes certain muscle cells and allows an increase of airflow to the lungs. Bronchodilators are treatments that work to expand the bronchi and decreasing resistance in the respiratory system. Albuterol is administered to patients experiencing bronchospasm, asthma, or other respiratory issues. Specifically, it activates pro-constrictoratory and pro-inflammatory pathways in human bronchial smooth muscle cell. Altered responsiveness of the beta 2 agonist expressed on airway smooth muscle are responsible for bronchodilation, increasing airflow to the lungs, in the treatment of respiratory constriction with Albuterol. Albuterol directly effects pathogens located on the smooth muscle cells. The airway   associated with the smooth muscle cells is responsible for many of the changes in airflow restrictions. When airways become restricted and cause reactions such as coughing or wheezing, it becomes known as bronchoconstriction. This bronchoconstriction is seemingly due to contraction agonists from inflammatory cells or reflex mechanisms. The mechanisms of airway smooth muscle cells are crucial for normal breathing function. When bronchial smooth muscle mass in enlarged due to abnormal bronchial smooth muscle cell increase, it leads to respiratory disorders. Mass of the cells can also become increased due to a build up of contractile proteins. Rapid reproduction of smooth muscle cells allow the airways to rejuvenate and becomes a target for anti-asthma agonists. During the absence of albuterol, pathogens along the smooth muscle cell lack the Beta-2 agonist which allow the muscles to become relaxed. The smooth muscle cells may contract independently when stimulated. Contractions in the smooth muscle are caused by the myosin light chain kinase. The pathway is triggered by an increase in intracellular calcium. The increase in calcium is sourced from the sarcoplasmic reticulum and also from the extracellular fluid through calcium channels. When calcium becomes increased, the Ca2+ ions can bind to a calcium binding protein, calmodulin. This creates a calcium calmodulin complex that activates the myosin light-chain kinase. Since the myosin light-chain kinase is activated, it is now able to phosphorylate myosin. Using ATP, it phosphorylates the heads on the myosin chain. This phosphorylation activates ATPase. The active ATPase moves along the thin filament using myosin head power strokes against the myosin filament. The cross bridges sliding along the actin create muscle tension. Because of this muscle tension, the myosin light-chain kinase pathway is characterised for its involvement in smooth muscle contraction. Albuterol is considered to be in the class of drugs that act specifically on the Beta 2 adrenergic receptor, allowing the smooth muscle cells to become relaxed. It is a bronchodilator that soothes muscles in the airways and increases air flow through the lungs. Its primary purpose is to treat the bronchospasm with people who have reversible obstructive airway diseases, such as asthma. Albuterol is a short term beta-2 agonist that mainly affects the muscles in the lung, such as bronchi. Patients’ lungs diagnosed with asthma can become irritated to the point where the bands of muscles surrounding the airway can become constricted and decrease airflow. Albuterol works to prevent and relax this constriction of the lungs.Albuterol is the common name for a group of beta-2 adrenergic agonist that activate the Beta 2 adrenergic receptor. Stimulation of the beta-2 adrenergic receptor is thought to be the primary receptor for controlling effects on the lungs. The Beta-2 adrenergic receptor is involved in the relaxation of bronchial smooth muscle. This is a receptor on airway smooth muscle cells, spanning the cell membrane. When the Beta-2 receptor is stimulated, its G-proteins become activated to dissociate to be able to release a protein subunit called Gs-alpha. The G protein subunit in turn activates a cyclic Adenosine monophosphate dependent subunit by activating adenylyl cyclase. The activated Adenylyl Cyclase causes a rise in intracellular cyclic adenosine monophosphate levels. This rise in cyclic adenosine monophosphate levels result in the majority of Beta-2 adrenergic effects. After cyclic adenosine monophosphate levels have risen, it prompts cyclic AMP-independent effects of Gs-alpha on the calcium activated potassium channel; as well as activation of protein kinase A. Protein Kinase A inhibits the phosphorylation of myosin and lowers intracellular ionic calcium concentrations, resulting in relaxation. A human’s respiratory smooth muscle cells should be in a natural state of relaxation. Only when the muscles become irritated or enlarged, is there a need for a beta-2 agonist to artificially allow the muscles to return to its normal state.