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Phys Lect 16

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.
Created by: WeeG



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