L19 Local Regulatory Mechanisms Flashcards
How does smooth muscle contract?
Smooth muscle depends on Ca-Calmodulin. When there is abundant Ca, it binds to Calmodulin. Ca-Calmodulin phosphorylates myosin-light-chain kinase, which turns the Myosin ON and contraction can happen.
MLC Phosphatase deactivates the MLCK and thus –> relaxation
Resistance vessels
Arterioles Precap sphincters (highest WT to lumen diameter ratio -- most control over dilation/constriction) metarterioles - a bridge for when you want to bypass cap beds
all things that regulate flow to something
Autoregulation
the body’s ability to maintain constant BF despite changes in BP
Regulates the BF by regulating resistance/diameter
Happens under resting conditions – can be overridden
Myogenic Hypothesis of AUTORegulation
A type of Autoregulation that says that when a vessel is stretched by in increase in transmural P, it reacts by constricted. When it shrinks, it dilates.
Hypothesis: stretch of the muscle activates membrane Ca channels.
Does the opposite thing that happens to it
Metabolic Hypothesis of AUTORegulation
Metabolically active tissues release metabolites, which cause vasodilation.
Increased BF whisks these away, so the vessel constricts.
If there isn’t much BF, metabolites stick around and dilate the vessel
Metabolic Regulation (Active and Reactive)
This is the normal type of vasodilation response. Occurs in EXERCISE.
1) Active hyperemia - normal vasodilation that occurs when BF goes up when the tissue is more and more active
2) Reactive hypermia - a reaction to when thee is an OCCLUSION. The occluded side builds up with metabolites and dilates - when the occlusion is removed, BF flows rapidly (overshoots) until all the metabolites are washed away
Mechanical Tissue Pressure
Increase in tissue P (ie isometric contraction in <3, Sk.m.) can cause small vessels to be compressed
Large contraction in heart like when it has a high overload could increase the amount of contraction necessary and this could compress vessels going to the endocardium (small)
Vasoconstrictors
Alpha-1 receptors
endothelin
Vasodilators
EDRF
NO
adenosine
histamine
SHOCK - when BP drops and BF to organs isn’t adequate
Cardiogenic - heart can’t pump out enough blood, CO down
Septic - infection in the blood - massive vasodilation, increased cap permeability, reduced R, LOW BP
Anaphylactic - allergic response causes massive vasodilation - could lead to obstruction of breathing, low BP
Hypovolemic - loss of blood, systemic reduce of BP (burns, vomiting, diarrhea, hemorrhage)
Neurogenic - when the ANS connections to vasoconstriction are lost; now everything is vasodilated
Endothelial Regulation
Increase in shear stress against the vessel wall induces the endothelium to release metabolites and other things that dilate the vessel.
This occurs when a P gradient is involved, meaning there is MORE FLOW. This DOES NOT occur when a static increase in pressure across the entire vessel is seen (this is regular autoregulation)
What happens when you stand up?
Gravity brings blood down to your lower extremities, but your BF stays constant due to Myogenic response –> the pre-capillaries are stretched by increase in P, so they constrict in response