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- W4213009324 abstract "The single unit smooth muscles and cardiac muscle do not have individual innervations but have gap junctional connections between individual cells and act as one sheet in a coordinated fashion in contrast to skeletal muscle. The depolarization in the pacemaker cells initiates synchronous depolarizations, which can be modulated by autonomic nervous system. In the heart, the sympathetic stimulation raises cyclic AMP and Ca2+ levels in myocardial cells and increases excitability of the cells, but ACh from the parasympathetic nerve to pacemaker cells decreases cAMP and Ca2+ levels and causes hyperpolarization in a resting state and reduces the pulse of heart through signal transduction pathways via Gα and Gβγ. If ATPase in the myosin head becomes more active at lower concentration of Ca2 +, the muscle fibers would get more excitable and induce arrhythmias. The pacemaker activity of intestine can be modified byan increasing theCa2 + via opening of IP3-gated Ca2 + channels and voltage-gated Ca2 + channels, thereby activating myosin ATPase “as seen in parasympathetic stimulation” and by decreasing affinity between the light-chain kinase and Ca2 +-CaM, thereby inactivating myosin ATPase “in sympathetic stimulation.” The second messenger in this case is triphosphate, diacylglycerol, and Ca2 + instead of cyclic AMP and Ca2 + in thd Ca2 + The increase in cytosolic Ca2 + leads to phosphorylation of the myosin light-chain at serine, which induces activation of the myosin ATPase. In healthy lungs, ACh by both neuronal and nonneuronal sources acts through muscarinic receptors to regulate physiological functions." @default.
- W4213009324 created "2022-02-24" @default.
- W4213009324 creator A5032630701 @default.
- W4213009324 date "2022-01-01" @default.
- W4213009324 modified "2023-09-28" @default.
- W4213009324 title "Mechanism of muscle contraction and disorder" @default.
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- W4213009324 doi "https://doi.org/10.1016/b978-0-323-98803-2.00008-0" @default.
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