Describe the relationship between membrane potential and force generation in tonic contractions and phasic contractions in smooth muscle. How do slow waves in smooth muscle relate to smooth muscle contractile responses?
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Smooth muscle cell (SMC) contraction is controlled by the Ca2+ and Rho kinase signalling pathways. While the SMC Rho kinase system seems to be reasonably constant, there is enormous variation with regard to the mechanisms responsible for generating Ca2+ signals. One way of dealing with this diversity is to consider how this system has been adapted to control different SMC functions. Phasic SMCs (vas deferens, uterus and bladder) rely on membrane depolarization to drive Ca2+ influx across the plasma membrane. This depolarization can be induced by neurotransmitters or through the operation of a membrane oscillator. Many tonic SMCs (vascular, airway and corpus cavernosum) are driven by a cytosolic Ca2+oscillator that generates periodic pulses of Ca2+. A similar oscillator is present in pacemaker cells such as the interstitial cells of Cajal (ICCs) and atypical SMCs that control other tonic SMCs (gastrointestinal, urethra, ureter). The changes in membrane potential induced by these cytosolic oscillators does not drive contraction directly but it functions to couple together individual oscillators to provide the synchronization that is a characteristic feature of many tonic SMCs.
Smooth muscle cells (SMCs) are characterized by their phenotypic plasticity and diversity. The activation mechanisms that control contraction display a similar diversity in that each SMC type has a signalling system that is uniquely adapted to control its particular function. The aim of this perspective is to confront this diversity by considering how the activation mechanisms for generating Ca2+ signals have been adapted to control different SMC functions.
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Smooth muscle cells (SMCs) are characterized by their phenotypic plasticity and diversity. The activation mechanisms that control contraction display a similar diversity in that each SMC type has a signalling system that is uniquely adapted to control its particular function. The aim of this perspective is to confront this diversity by considering how the activation mechanisms for generating Ca2+ signals have been adapted to control different SMC functions.
hope..it....helps..
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