Local Control Of Vasculature Flashcards
Alpha1-adrenergic receptors
Located in arterioles and arteries
Vasoconstriction
Beta1-adrenergic receptors
Heart
Increase CO
Beta2-adrenergic receptors
Lungs and skeletal muscle
Vasodilation
M2 receptor
Heart
Decreases CO
Cholinergic
Eph/NE effect on vasculature
Epinephrine: released by adrenal gland
Activates beta-1 in heart (increase CO), beta-2 (vasodilation in skeletal muscle), and alpha-1 (vasoconstriction in arterioles, arteries)
NE: released from sympathetic terminals
Activates alpha-1 (veins and arterioles) —> vasoconstriction
Vasoconstriction (sympathetic) is tonically active…basically always happening…increases bp and mobilizes blood volume
Anaphylactic reaction (like eating peanuts when allergic)
Systemic vasodilation due to histamine reaction (and broncho-constriction)
Epi - pen is best and quickest treatment
***not NE because not as good for treating broncho-constriction
Stimulation of D1 receptors by dopamine
Vasodilationg and natriuresis in the renal tubules
Dopamine can also activate alpha1 and beta1 receptors
Role of adenosine, H+, CO2, and K+ in promoting vasodilation
Signs of active cells…therefore need vasodilation to promote filtration
These metabolites diffuse towards the arterioles, interacting with SmM…receptors that recognize adenosine —> release cAMP to vasodilate
Drop in O2 and rise in CO2 = ischemia —> promotes vasodilation
Factors that lead to smooth muscle dilation
Decreased cytosolic Ca2+
Hyperpolarization
Increase cAMP, cGMP
Increased EC K+
Nitric oxide
Leads to vasodilation
Works fast and effective, short 1/2 life
Released by endothelial cells when they detect an increase in shear stress
Release can be caused by histamine, bradykinin, serotonin, ATP, stress
L-arginine —> NO —> (goes to SmM) —> guanylyl cyclase —> increase in cGMP —> increase K+ efflux —> dilation
Another mechanism (independent of endothelium):
Sodium nitroprusside releases NO upon binding to oxyhaemaglobin —> increase in cGMP…
Prostacyclin (PGI)
Same effect as Nitric Oxide, but not as effective
Response to shear stress and bradykinin —> COX and PGI Synthase stimulated —> PGI —> (goes to SmM) —> increase cAMP —> relaxation
PGI’s major function is to inhibit platelet aggregation
Endothelin
Released by endothelial cells, when they sense signals for vasoconstriction
Like…angiotensin II, ADH, cytokines, reactive O2 species,
Or turbulent flow
Stimulates IP3 production —> release of SR Ca2+ stores and vasoconstriction
How arterial blood vessels going to brain, with resting myogenic tone, respond to increases in bp
Drop in pressure —> vasodilate as a response —> reduces resistance of blood flow downstream —> keeps volume of blood going to brain constant
Spike in pressure —> vasoconstrict…increase resistance
Limit of myogenic response
Flow is held constant until you reach this limit…then blood flow shoots all the way up
Higher tone = better ability to maintain a constant flow
Strongest tone = cerebral vasculature
Autoregulation (intrinsic) mechanisms that lead to vasodilation
Metabolic:
decrease O2 Increase CO2 Decrease pH Increase EC K+ Prostaglandins Adenosine Nitric oxide
