Smooth Muscle Flashcards
Innervation of smooth muscle
-ANS
Smooth muscle differences:
- slower movements
- monomnucleated
- actin/myosin not organized into sarcomeres, instead they run parellel to the long axis of the cell (contractile filament domains)
- much more MYOSIN than actin (allows for more shortening, less volume but generates greater force due to the length)
- are some of the smallest cells in the body
- NO TROPONIN, caldesmon or calponin instead
- develop LATER, from non-muscle cells
Actin and Myosin organization in smooth muscle
-into groups of overlapping filaments within the cells
Cross bridge cycling in smooth muscle
- myosin is morphologically same as skeletal but biochemically different
- ATPase normally OFF and must be turned on, activation due to phosphorylation of myosin light chain
- calcium influx activates calmodulin which activates the MLCK which phosphorylates ATP and activates myosin
- only need about 50% of the sites activated for the system to be maximum
Junctions between smooth muscle cells:
simple opposition
intermediate contact
desmosome
gap junction
Calcium sources for smooth muscle contraction
1) electromechanical coupling: entry of calcium via voltage gated calcium channels (L type) *action potential
2) pharmacological coupling: receptor-operated calcium channels or SR release
SR release of calcium in smooth muscle
- not due to depolarization but triggered by PLC - PIP2 — IP3 second messengers
- smooth muscle can contract without a change in membrane potential
- ACh is one type of agonist/receptor for this
- SR amount varies
How does smooth muscle force vary with MLC phorphorylation?
- increased phorphorylation = increased tension
* smooth muscle is never totally relaxed
Relationship between action potential and the number of SR
- vascular smooth muscle has no action potential and therefore an increased number of SR
- GI has less SR because action potential used
Regulation of smooth muscle contraction:
- is accomplished via inhibition of MLCP
- via activation of MLCK via calcium
Regulation of smooth muscle relaxation:
- accomplished via activation of phosphatase
- via inactivation of MLCK activity (decrease calcium)
Agonist activation of smooth muscle:
relies on MLCP inactivation
- GP activation of rho activates rho kinase which phosphorylates the myosin binding site of MLC phosphatase = INACTIVATION
- Protein kinase C can also inactivate via CPI-17
How to activate MLCP
- subset of smooth muscle used NO which increased cGMP which activates PKG which bind/activates MLCP
- desensitized to calcium levels, mechanism of Viagra
Beta-receptor stimulated decrease of MLCK
-increased cAMP leads to phosphorylation of MLCK which DECREASES activity
- asthma treatment shuts down MLC and relaxes
- via beta agonist
How to decrease calcium during relaxation
- take away agonist
- stop membrane depolarization