Increase in cytosolic calcium from intracellular storage, during smooth muscle contraction is/are due to:
D i.e. IP3- DAGDuring smooth muscle contraction increase in cytosolic calcium is due to influx through voltage or ligand gated plasma membrane Ca++ channelsQ and release of Ca++ from sarcoplasmic reticulum activated by 1P3 receptor calcium channelsQ- Different source of calcium- As in skeletal & cardiac muscle, Ca++ plays a impoant role in initiation of contraction but the source of Ca.* increase is much different- Unlike skeletal & like cardiac muscle most of the calcium which enters sarcoplasm comes from ECF and very little comes from sarcoplasmic reticulumQ. So the source of ca-- are:Phosphorylation of myosin is essential for its binding to actinLack of troponin in smooth muscles prevents Ca'* activation troponin binding. Rather Ca** binds to calmodulin and resulting complex activates calmodulin dependent myosin light chain kinase (MLCK). This enzyme catalyzes the phosphorylation of myosine light chain on serine at position 19Myosin LC20 phosphorylation is a must and increases myosin ATPase activityQ resultingin binding of myosin to actin and contraction . However, phosphorylation & dephosphorylation of myosin also occur in skeletal muscle but phosphorylation is not necessary for activation of ATPaseDephosphorylation & Latch bridgesMyosin LC is dephosphorylated by myosin light chain phosphatase but it does not necessarily Vt relaxation & final detachmentQ of myosin cross bridges from actin until the intracellular concentration of falls below a critical level.This continued attachment of myosin cross bridges to actin even after dephosphorylation creates latch bridgesLatch bridges do not make significant cycles of attachment & detachmentQ between actin & myosin so do not require much ATPQ and so maintain prolonged contractions without expenditure of much energy.If epinephrine or NE is added, the membrane potential becomes larger, the spikes decrease in frequency & muscle relaxes. Whereas acetylcholine addition 1/t decreased membrane potential, spikes become more frequent, muscle becomes more active with an increase in tonic tension & number of rhythmic contractions.During smooth muscle contraction increase in cytosolic calcium is due to influx through voltage or ligand gated plasma membrane Ca++ channelsQ and release of Ca++ from sarcoplasmic reticulum activated by 1P3 receptor calcium channelsQ
CAMP
CGMP
CCMP
IP3- DAG