Smooth Muscle Flashcards
What are the main ways that smooth muscle get Calcium entry?
- Voltage gates calcium channels in t tubules from AP
- Stretch receptors
- Neurotransmitter/hormonal
- CICR from sarcoplasmic reticulum
- SOCE when SR is depleted
Main differences between smooth muscle and skeletal muscle?
Smooth Muscle
- Smaller than skeletal
- Single nucleated
- Not organized into tight sarcomeres, so no striations
- Still use actin and myosin
- Contraction speed is slower
- Contraction time is longer
Explain the steps in smooth muscle contraction
- Increase in intracellular calcium
- Calcium binds to calmodulin
- Ca/Cam binds with Myosin light chain kinase
- Phosphorylates myosin light chain
- Crossbridge cycling occurs
Explain steps of smooth muscle relaxation
- Can change contraction by altering levels of Ca2+ and myosin phosphatase activity
- For relaxation the cell needs to have low Ca2+ and increased myosin phosphatase activity
Note: Binding of ATP to the myosin heads is slow, can sustain contractions
What is the role of endothelium in vascular smooth muscle relaxation?
It releases nitric oxide that causes smooth muscle relaxation
-One of the first signs of vascular disease is a decrease in NO
Adrenergic and cholinergic receptors in blood vessels
What normal degrades cGMP? What drug inhibits this?
Phosphodiesterases (PDE5)
Viagra inhibits this, leads to more vasodilation
What happens when NE binds to alpha 1 receptors on vascular smooth muscle of blood vessels?
- GPCR pathway is activated
- Gq -> PLC -> IP3(second messenger) -> increase Ca2+
- Increases myosin and actin interaction
- Increase contraction of smooth muscle (vasoconstriction)
What happens when there are sympathetic effects on smooth muscle around some blood vessels on B2 receptors?
- GPCR is activated
- Gs -> Adenylyl cyclase -> ATP is converted to cAMP(second messenger)
- cAMP inhibits MLCK
- Decreases actin and myosin interaction
- Decreases contraction of smooth muscle (vasodilation)
What are the parasympathetic effects on vasculature?
First of all there are Ach receptors on the endothelium and smooth muscle
- Ach releases NO from endothelium, once in blood vessels it causes vasodilation
- Ach can also directly cause smooth muscle contraction (IP3)
What are the sympathetic effects on B2 receptors in bronchiole smooth muscle?
Epinephrine >> Norepinephrine
- Gs -> Adenylyl cyclase -> cAMP -> PKA -> closes Ca2+ channels
- Decrease in myosin and actin interaction
- Decrease in contraction of smooth muscle (bronchodilation)
What are the parasympathetic effects on smooth muscle in bronchioles?
- Ach binds to muscarinic receptors
- Gq -> PLC -> IP3 (second messenger) -> Increase Ca2+
- Increase in smooth muscle contraction (bronchoconstriction)
What are some paracrine/local factors that cause vasodilation of smooth muscle?
High CO2
High H+
NO
What are some endocrine factors that can affect smooth muscle excitation/relaxation?
- Hormones
- Angiotensin II, endothelin, vasopressin, serotonin, histamine
- Bind to a receptor and open ion channels, etc. that causes depolarization or hyperpolarization
- Self excitation/pacemaker