Smooth Muscle Contraction Research Paper

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Neural Regulation, EC Coupling, and Second Messenger System involvement with Bronchial Smooth Muscle Contraction and Relaxation

Abstract Smooth muscles in human airways have multiple pathways for excitation and contraction. Both electrical and chemical signals regulate bronchial smooth muscle excitation. Bronchial smooth muscle is innervated by parasympathetic cholinergic nerves for contractile forces and by parasympathetic noncholinergic nerves for relaxant forces. Specifically, cholinergic nerves that secrete acetylcholine to muscarinic receptors cause smooth muscle excitation and adrenergic nerves that emit catecholamines to adrenoceptors result in smooth muscle inhibition. There are varied neural and chemical receptors that begin these reactions. Bronchial smooth muscle is unique in that it has specific receptors on the plasmolemma that do not respond to stimuli the same way that other airway smooth muscle cells do. This means the stimulus that would normally start contraction has no effect on bronchial smooth muscle. Bronchial smooth
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Airway smooth muscles are innervated by two different nerves. The preganglionic parasympathetic nerves originate from the vagus nerve and the postganglionic sympathetic nerves originate from the thoracic and cervical ganglia (1). These nerves can be either excitatory or inhibitory. The postganglionic sympathetic nerve is the only pathway that does not use acetylcholine as a neurotransmitter, but instead uses norepinephrine. While the ASM contains nerves from both the parasympathetic and the sympathetic nervous systems, the muscles are only directly regulated from the parasympathetic nerves. While postganglionic sympathetic nerves are present, they do not transmit norepinephrine directly to the smooth muscle—the norepinephrine that is available is circulating freely among the tissue, secreted from the adrenal medulla

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