Smooth muscle contraction Flashcards
(21 cards)
Smooth muscle dependent on
Ca/K AP
- extracellular Ca- unlike skeletal muscle
Caveolae
On surface of sarcolemma
- have Ach and adrenergic receptors
- Ion channels- L-type Ca channels- ATP sensitive K channels- Ca sensitive K channels
Smooth muscle action potential
Ca dependent
- inward depolarizing current is carried by calcium ions
- –NOT Na ions
Unitary
Single unit smooth muscle
- Electrically coupled via gap junctions
- contract as single unit
Multiunit
Discrete smooth muscle fibers
-each innervated by a single nerve ending
Ca binding to calmodulin
Causes contraction
key regulatory protein- Myosin light chain kinase (MLCK)
-Phosphorylation of the regulatory light chain changes conformation allowing interaction with actin
Smooth muscle relaxation
Phosphatase in sarcoplasm- dephosphorylates the regulatory light chain of myosin- interaction btwn actin and myosin is blocked
Also- reduction of calcium by the calcium ion pumps
Electromechanical smooth muscle contraction
APs and stretch- Ca channels open
Pharmacomechanical
Ligand binding to cell surface receptors
-G-protein– PLC— IP3–IP3 receptors opening in SR
Intestine/stomach/colon/uterus
develop synchronous contractions and pacemakers with diastolic depolarizations
Basal electric rhythm (BER)
Waves of rhythmic depolarization of intestinal smooth muscle cells
-originate at specific point then propagate
Cells of Cajal in stomach
Release of NT from enteric nerve creates AP
- leads to contraction
- important for peristalsis
Latch bridge state
Muscle maintains tension
- MLCP dephosphorylation of the myosin light chain while the myosin head is bound to actin
- If its dephosphorlated while head is detached then the myosin is inactive and cross bridge cycle ends
Endothelin (ET-1)
Produced by vascular endothelium
once released it binds receptors
-ETa
-ETb
ETa
Dominant in blood vessels
-responsible for contraction
ETb
found in endothelium
- NO stimulated when ET-1 binds
- causes vasodilation
Cardiovascular effects of endothelin
Systemic administration of ET-1 causes transient vasodilation and hypotension– ETb activation
- Followed by prolong vasoconstriction and HTN
- –ETa and ETb activation
Dzs associated with elevated endothelin
HTN
coronary vasospasm
heart failure- ET-1 released by failing myocardium- contributes to Ca overload and hypertrophy
Pulmonary HTN- ET-1 antagonist Bosentan used to treat
Release of Epi from adrenal medulla causes
Vasoconstriction in most arterioles
-Skin and gut
Vasodilation in the arterioles of the skeletal muscle and heart and bronchiolar smooth muscle in the lungs
A1 adrenalin receptor
Binding of epi leads to vasoconstriction
-found in all arterioles
IP3 and Ca release- myosin phosphate active– contraction
B2 adrenalin receptors
Binding of epi leads to vasodilation
cAMP- PKA- phosphorylates MLCK- inactivates MLCK
-Prevents MLCK from being activated by Ca release
-Cause relaxation