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    How does a stimulus leads to the contraction smooth muscle membrane without a change in the membrane potential?

    This can occur by two key methods:

    - Modulation of intracellular calcium concentration
    - Modulation of Myosin light chain phosphorylation

    The signals are transduced by GPCRs. Stimulation of for example the M3 AChR (which is Gq coupled) raises intracellular calcium via the signalling molecule IP3 acting on the endoplasmic reticulum to cause release from stores. The calcium forms complexes with calmodulin which activate MLCK (myosin light-chain kinase), permitting cross-bridge cycling to occur.

    Relaxation can be mediated by Gs coupled GPCRs such as the IPR and B-adrR. Increasing PKA activity as a result causes a reduction in intracellular calcium (PLB etc.) and a reduction in sensitivity to it. It also stimulates MLCP ( '' '' '' phosphatase) to dephosphorylate myosin to reduce cross-bridge cycling. This can affect membrane potential, but is not wholly dependant on it.

    Of course smooth muscle is extremely complicated, but the key principle is that intracellular calcium can be raised by its release from intracellular stores which is not dependant on depolarisation of the plasma membrane and subsequent calcium entry through it. It is dependant on signalling through GPCRs. The calcium then acts as a signalling mediator for contraction be a number of pathways.
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Updated: April 10, 2011

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