| Question | Answer |
| 3 ways to remove Ca2+ from cytosol? | 1.Ca ATPase.
2.Na-Ca Antiporter.
3.SERCA Pump |
| Steps for relaxation in smooth muscle | 1.Remove Ca2+ from cytosol.
2.Dephosphorylation of myosin head by MLCP (Inc by PKG or PKA).
3. |
| MLC Phosphorylation in Phasic contractions | MLCK and MLCP are phos/dephos the myosin head cross-bridges with every contraction.
**Ca2+ levels also go up and down with each contraction |
| Tonic contraction: Latch state | is a way for smooth muscle to conserve ATP by dephosphorylating the MLC while the myosin head is still forming the cross-bridge. This maintains force through cross-bridges while decreasing ATP hydrolysis.
**Can economically stay contracted much longer |
| Velocity of contraction during Latch State | 0. b/c the ATP hydrolysis has been reduced, the cross-bridge cycling of normal isotonic contractions will slow making the rate of cycling 0.
**Latch State only maintains FORCE, no velocity |
| Intracellular [Ca2+] and cross-bridge phosphorylation in Tonic Vs Phasic contractions | 1.Phasic: Both cycle up and down with AP and contraction.
2.Tonic: Ca2+ and c-b phosphorylation go up with AP, but do not return back to base line when the AP leaves. This allows a longer, static force generation. |
| If an increase in MLCK? MLCP? | 1.MLCK: Net Phosphorylation of MLC.
2.MLCP: net dephosphorylation of MLC. |
| Regulation of smooth muscle contraction | Since initiation is a 2 step process, either of the 2 steps can be regulated:
1.[Ca2+].
2.MLCK/MLCP |
| Main secondary messanger invovled in smooth muscle hormone induced relaxation | cAMP |
| Main secondary messanger invovled in smooth muscle hormone induced contraction | IP3 |
| Epi/Norepi: Smooth Muscle contraction | 1.Receptor: Alpha1.
2.Secondary Messanger: IP3 |
| Epi/Norepi: Smooth Muscle relaxation | 1.Receptor: Beta2.
2.Secondary Messanger: cAMP |
| ACh: Smooth Muscle contraction | 1.Receptor: mAChR
2.Secondary Messanger: IP3 |
| ACh: Smooth Muscle relaxation | 1.Receptor: mAChR/EC
2.Secondary Messanger: NO |
| Angiotensin II: Smooth muscle contraction | 1.Receptor: AT1
2.Secondary Messanger: IP3 |
| Vasopressin: Smooth muscle contraction | 1.Receptor: V1
2.Secondary Messanger: IP3 |
| Endothelin: Smooth Muscle contraction | 1.Receptor: ETa
2.Secondary Messanger: IP3 |
| Adenosine: Smooth muscle relaxation | 1.Receptor: A2
2.Secondary Messanger: cAMP |
| PKA | Inhibits MLCK, which will induce smooth muscle relaxation. |
| PKC | Inhibits MLCP, which will induce smooth muscle contraction. |
| PKG | ACTIVATES MLCP, which will induce smooth muscle relaxation. |
| Endothelial cells' effects on vascular smooth muscle | Endothelial cells release several hormones that alter the smooth muscle:
1.NO: relaxtion/ vasodilation.
2.Prostacyclin: relaxation/ vasodilation.
3.Endothelin: conraction/ vasoconstriction. |
| Mechanism behind ACh or Bradykinin causing vasodilation | 1.ACh binds to mAChR or EC receptor on endothelial cell.
2.Ca2+ influx
3.NO is activated as secondary messanger.
4.NO released from endo cell.
5.Activates GC in sm
6.Activates PKG
7.Inc MLCP & vascular sm relaxation. |
| How does length-tension relationship for smooth muscle differ from striated muscle? | It is a broader curve indicating it can form cross-bridges and generate tension over a wider range of lengths.
**curves still look similar b/c the actin-myosin overlap principle is the same |
| How does load-velocity relationship for smooth muscle differ from striated muscle? | it is less steep in smooth muscle.
**Directly dependent on MLCK because MLC phosphorylation increases the rate of ATP hydrolysis and increases the velocity. |
