Pig Trachealis Smooth Muscle Pharmomechanical coupling uses Internal Calcium stores whilst Electromechanical coupling uses Extracellular Calcium
Pig Trachealis Smooth Muscle Pharmomechanical coupling uses Internal Calcium stores whilst Electromechanical coupling uses Extracellular Calcium
Crystal Nguyen
School of Anatomy, Physiology and Human Biology, The University of Western Australia, WA, 6009
Introduction
Smooth muscle contraction occurs when calcium is present in the smooth muscle cell and binds onto calmodulin to activate myosin light chain kinase (Wilson et al., 2002). Phosphorylation of myosin light chains result in myosin ATPase activity thus cross-bridge cycling occurs causing the muscle to contract (Horowitz et al., 1996). There are two known models of excitation and contraction in smooth muscle, electromechanical coupling (EMC) and pharmomechanical coupling (PMC) (Droogmans et al., 1997). EMC involves a change in membrane potential as a result of nerve stimulation (Sanders, 2008). Depolarisation causes voltage gated calcium channels to open and contraction occurs. High potassium (K+) concentration causes potassium leak channels to shut down thus no positive charge leaves the cell and the membrane becomes depolarised (Morgan et al., 1981). It is possible to determine if a tissue uses EMC, by depolarising the tissue and seeing if it contracts. Depolarisation of smooth muscle cells through the EMC can be achieved when a K+-depolarisation solution is used as a stimulus, causing calcium release and contraction. On the other hand, PMC does not require a change in membrane potential (Edman, 1962). Rather, drugs mediate smooth muscle contraction, for example acetylcholine (Ach) that bind onto receptors and cause the calcium into the smooth muscle cell causing it to contract (Devine et al., 1972, Sanders, 2008).
It is known that the two pathways, EMC and PMC result in smooth muscle contraction; however, the source of calcium required for contraction is unknown for each pathway. Therefore, this study aimed to investigate whether the use of calcium in EMC and PMC relies on external or
Crystal Nguyen
School of Anatomy, Physiology and Human Biology, The University of Western Australia, WA, 6009
Introduction
Smooth muscle contraction occurs when calcium is present in the smooth muscle cell and binds onto calmodulin to activate myosin light chain kinase (Wilson et al., 2002). Phosphorylation of myosin light chains result in myosin ATPase activity thus cross-bridge cycling occurs causing the muscle to contract (Horowitz et al., 1996). There are two known models of excitation and contraction in smooth muscle, electromechanical coupling (EMC) and pharmomechanical coupling (PMC) (Droogmans et al., 1997). EMC involves a change in membrane potential as a result of nerve stimulation (Sanders, 2008). Depolarisation causes voltage gated calcium channels to open and contraction occurs. High potassium (K+) concentration causes potassium leak channels to shut down thus no positive charge leaves the cell and the membrane becomes depolarised (Morgan et al., 1981). It is possible to determine if a tissue uses EMC, by depolarising the tissue and seeing if it contracts. Depolarisation of smooth muscle cells through the EMC can be achieved when a K+-depolarisation solution is used as a stimulus, causing calcium release and contraction. On the other hand, PMC does not require a change in membrane potential (Edman, 1962). Rather, drugs mediate smooth muscle contraction, for example acetylcholine (Ach) that bind onto receptors and cause the calcium into the smooth muscle cell causing it to contract (Devine et al., 1972, Sanders, 2008).
It is known that the two pathways, EMC and PMC result in smooth muscle contraction; however, the source of calcium required for contraction is unknown for each pathway. Therefore, this study aimed to investigate whether the use of calcium in EMC and PMC relies on external or
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