Excitation-Contraction Coupling in Smooth Muscle-Smooth muscle can be excited to contract by:o Pacemaker cells- are intrinsic to the smooth muscle; they spontaneously depolarize generating action potentials to stimulate smooth muscle contractiono Chemicals- have receptors expressed on smooth muscle cells; chemicals such as:o Neurotransmitterso Hormones * Skeletal muscle contraction is by excitation of a motor neuron; skeletal muscle lacks pacemaker activity and lacks stimulation by chemicalso Autonomic nerve fibers- the bulbous swellings of the autonomic fibers called varicosities form junctions with smooth muscle called diffuse junctions. When the autonomic nerve fibers are activated, the neurotransmitter released may stimulate the smooth muscle to contract or relaxo Unlike skeletal muscle, activation of autonomic NS may cause smooth muscle contraction or smooth muscle RELAXATIONo Smooth muscle in the walls of the bronchioles (tube-like structures that transport air in/out of the lungs)o Activation of the parasympathetic NS to the bronchioles results in contraction of the smooth muscle in the walls of the bronchioles bronchoconstrictiono If the sympathetic NS is activated, results in relaxation of the smooth muscles in the walls of the bronchioles bronchodialation, this will act as a basis for using sympathomimetic drugs to manage asthmaSequence of events in the mechanism of Smooth Muscle Contraction1. Action potentials develop at sarcolemma of smooth muscle by pacemaker activity, a chemical, or autonomic nerve fiber2. Action potentials at sarcolemma cause Ca2+ channels to open at the sarcolemma; activation leads to increase in intracellular calcium ions (Ca2+ goes down its concentration gradient and enters the smooth muscle cells from the extracellular fluid in the caveolae and also by release from poorly-developed SR (unlike SR in skeletal muscle fiber, SR in smooth muscle cells do not contain enough Ca2+ to support contraction of smooth muscle cells); referred to as “calcium-entry calcium trigger mechanism”a. So, increase in Ca2+ in sarcoplasm from 2 sources- (1) extracellular fluid and (2) poorly developed SR3. Ca2+ binds to Calmodulin (skeletal muscle Ca2+ binds to TnC; troponin is absent from smooth muscle cells)4. Calcium-Calmodulin complex activates myosin light chain kinase (MLCK), which removes Pi from ATP and attaches Pi to the myosin globular heads5. Activated MLCK phosphorylates/activates the myosin heads to form cross bridges-attach to the accessible myosin binding sites on actin (although tropomyosin is present in thin filaments, it does not block myosin binding sites on actin)6. Upon attachment of cross bridges, sliding of thin filaments occurs=shortening of smooth muscle cells= smooth muscle contraction7. Cross bridge detachment occurs when the enzyme, phosphorylase, removes the phosphate from the myosin heads to return them to their resting state (inactivated state); **skeletal muscles require binding of NEW ATP to its site on the cross bridges for cross bridge
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