Smooth Muscle Flashcards
Describe smooth muscle
Function: to act as bodys conduits for transport of gases/liquids/gases
Morphology: Not striated, spindle shaped
Location: Walls of hollow organs including blood vessels
Regulation: Autonomic Nervous System , Hormones, GI tract- rhythmic contractions initiated by pacemaker cells
Examples of smooth muscle containing organs
GI tract- for mixing and propulsions of Gi contents
uterus- labour
Respiratory system- diameter of airways
Bladder/ureters- micturition, urine storage
Characteristics features of SMCs
Elongated shape
Lack of striations
Dense bodies are present, anchoring actin filaments
ER present- storing Ca++
GAP junctions between cells through which current and small molecules can flow
How is the contraction of smooth muscle regulated?
Vascular- ANS, autocoids, local hormones, vascular endothelium
(ACTION POTENTIAL PRESENT ONLY SOMETIMES)
Airways- ANS, autocoids, local hormone
(NO ACTION POTENTIAL)
Intestinal- intestinal cells of Cajal- pacemaker, ANS, local hormones
(ACTION POTENTIAL)
Bladder- ANS, autocoids, local hormones
(ACTION POTENTIAL)
Autocoids-
Physiologically active factor released by cells which typically acts locally and briefly on other cells
Local Hormone
Any regulatory substance released by cells acting in autocrine or paracrine fashion
Structure of a blood vessel
Smooth muscle wrap around the artery circumfrancially- makes up the tunica media
Endothelial cells sits on internal elastic lamina- they play an important role in contraction of smooth muscle
Internal elastic lamina- made up of elastin and has holes in it
Gap junctions present in the internal elastic lamina and tunica media which means that it stimuli can addict the endothelium and affect muscle cells
Vascular tone is the result of the balance between various constructing and dilating influences - give examples
Blood Bourne substances CONSTRICT ( through adrenaline or angiotensin II)
Local Hormones can either CONSTRICT or DILATE
Pressure/stretching CONSTRICTS
Sympathetic nerves- releases noradrenalines which CONSTRICTS
Flow and Blood borne substances release NO which DILATES
Metabolites DILATE
Vascular smooth muscle contraction
- Noradrenaline released from the sympathetic nerves that innervate blood vessels
- Binds to alpha receptors
- Through G-proteins, it activates phospholipase C- converting PIP2 to DAG and IP3
- IP3 releases Ca from its stores in ER. Ca++ pours out causing a contraction as CA++ concentration increases
DAG binds to receptor gated channels which allows NA+ and Ca++ to enter and so its concentration increase.
The CA++ can enter a different cell via gap junctions
- As positive charge enters, the membrane becomes depolarised which leads to AP
—– 3. The binding activation rhokinase which stimulates Ca++ sensitisation
NO mediated vasodialtion
- endothelial cells release NO
- NO diffuses into the cell by diffusion
- This activates an enzyme called GC which converts GTP to cGMP
- a) Phosphorylates K+ channels allowing K+ to leave. This means that the membrane becomes hyperpolarised. It will also reverse the Ca++ channels opening
4b) Phosphorylates SERCA which means that Ca++ is being actively pumped into the Sarcoplasmic reticulum
Phosphorylates PMCA which means calcium ions are being activated pumped outside the cell
4c) cGMP desensitises the Ca++
Adrenaline causing dilation
- Adrenaline binds to beta 1 receptor
- This activates AC which converts ATP to cAMP
- a) Phosphorylates K+ channels allowing K+ to leave. This means that the membrane becomes hyperpolarised. It will also reverse the Ca++ channels opening
3b) Phosphorylates SERCA which means that Ca++ is being actively pumped into the Sarcoplasmic reticulum
Phosphorylates PMCA which means calcium ions are being activated pumped outside the cell
Smooth muscle cross bridge cycle and its regulation
- Myosin + Calmodulin when there’s an Increase in [Ca++] forms an active complex.
This converts myosin to myosin phosphatase.
Myosin phosphatase forms a complex with actin as ATP is hydrolysed to ADP. This complex can be reconverted. ( FAST CROSS BRIDGE FORMING- generates force )
2 . Myosin phosphatase converts myosin phosphatase back to myosin.
Activated by NO via CGMP Ca++ desenstisation
Inhibited by agonists via rho kinase
Ca++ sensitisation which promotes contraction
Comment on why cross bridge cycling is much slower in smooth muscle compared to striated muscle is useful
Leads to a much Lower requirement of ATP synthesis
Smooth muscle doesn’t fatigue easily can be contracted indefinitely
Regulation of tension development in smooth muscle
Myosin phosphatase with actin can be converted to myosin actin complex which allows for the contraction to be maintained (latch bridges) - formed when myosin is dephosphorylated- the cycle here is very slow.
Allows for the maintaining of the force without ATP expedenture
