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Reading about smooth muscle cells, I stumbled upon this sentence in Guyton & Hall, Textbook of Medical Physiology (14th ed):

When the myosin kinase and myosin phosphatase enzymes are both strongly activated, the cycling frequency of the myosin heads and the velocity of contraction are great. Then, as activation of the enzymes decreases, the cycling frequency decreases but, at the same time, the deactivation of these enzymes allows the myosin heads to remain attached to the actin filament for a longer and longer proportion of the cycling period.

I'm having trouble reconciling this with myosin phosphatase's role. Elsewhere in the book it is stated that myosin phosphatase plays a role in smooth muscle contraction cessation, and that phosphorylated myosin (i.e. the product of myosin kinase) can, by itself, repeatedly attach to and detach from the thin filament and perform the cross-bridge cycles. As in, detachment of the myosin head from the actin filament does NOT require its dephosphorylation (via myosin phosphatase); and rather, the dephosphorylation only occurs when the cycling should stop altogether so that muscle relaxation occurs.

If this is true, then why would myosin phosphatase need to be 'strongly activated' (as per the quote above) so that the cycling frequency and velocity of contraction increases? Would that not actually reduce the cycling frequency? It seems to me that myosin kinase should be strongly activated and myosin phosphatase be strongly inhibited if the cycling frequency is to increase, but I'm probably misunderstanding something.

How does myosin phosphatase activation (or as the quoted part says, strong activation of both myosin kinase and myosin phosphatase) actually increase the cycling frequency?

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Simply cutting the calcium level will not revert the mechanism in case of Vascular Smooth Muscles. Due to absence of Troponin in their sarcomere.

For the reaction to go forward as well as backward we are dependent on MLCK and MLCP both respectively and to shorten the time period(increase frequency) we need to raise the concentration of both.

Citation & Explanation

Unlike skeletal muscle, smooth muscle is phosphorylated during its activation, which creates a potential difficulty in that simply reducing calcium levels will not produce muscle relaxation.(Section:Mechanism Paragraph 3rd).

Citation: https://www.ncbi.nlm.nih.gov/books/NBK526125/

This is due to absence of troponin which is present in Cardiac Smooth Muscles and Skeletal Muscles but not in vascular smooth muscles.

Citation:https://pubmed.ncbi.nlm.nih.gov/12665242/ Citation:https://cvphysiology.com/Blood%20Pressure/BP026 (check paragraph 1 and the Image shown on the page)

Thank You

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  • $\begingroup$ For the reaction to go forward as well as backward we are dependent on MLCK and MLCP both What is this 'reaction' that needs to go backwards? I don't understand what muscle relaxation has to do with the cycling frequency. Doesn't relaxation (via MLCP) happen AFTER the cycling is done? I'm asking about how increased MLCP activity is needed for the contraction itself (i.e. the cross-bridge power-stroke cycles that occur during the contraction), not why MLCP is required for contraction (and the entire cycling mechanism) to stop. $\endgroup$ Aug 22, 2022 at 12:52
  • $\begingroup$ pubmed.ncbi.nlm.nih.gov/9887960 this is the paper which you'll probably find the answer, i will post my updated answer after reading it. $\endgroup$
    – daemon
    Aug 22, 2022 at 14:17

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