Local Control of BP Flashcards
Myogenic Autoregulation
- Intrinsic ability of vascular smooth muscle cells to regulate own activity
- Goal = maintain constant flow (Q) = maintain constant O2 delivery
- If pressure inc, smooth muscle dec radius/inc resistance to maintain flow (Q)
- How?
- Independent of nervous system
- Rise in pressure —> stretch wall of vascular smooth muscle cells —> open stretch-sensitive Na+ channels —> depolarization —> open voltage-gated L-type Ca++ channels —> more Ca++ in cell —> contract/vasoconstrict
Which metabolites cause vasodilation? (4 ex)
- H+ (acidic), K+ and CO2 trigger vasodilation (all esp released in working muscle)
- If low O2 —> triggers adenosine —> inc cAMP —> PKA —> phosphrylate/act K-ATP channel —> K+ efflux/hyper-polarization (RELAX)
- High extracellular K+ causes IKr channel to open —> K+ efflux —> hyper polarization
Endothelin
released from damaged endothelial cells —> vasoconstriction (reduce bleeding)
Serotonin
released from activated platelets —> vasoconstriction (also reduce bleeding)
Histamine
released from mast cells once clot/plug has been formed —> vasodilation (get molecules to site)
3 Ways NO is produced
1- If sheer stress of blood parallel to vessel
* Stress —> opens mechanically-gated Ca++ channels on surface —> Ca-Calmodulin —> activates NO synthase
* Other mechanically-gated channels —> kinase cascade —> phosphorylate NO synthase so MORE ACTIVE
2- Bradykinin from cell damage also causes NO release from endothelial cells —> inc flow to repair damage
3- RBCs
* More O2 delivery = more blood flow to that tissue
* As RBC deliver O2 they now have open HB which acts as a reductase of NO2- —> O2
* When O2 is delivered the RBC also make ATP via glycolysis —> release of ATP triggers release of NO from endothelial cells
How does NO cause vasodilation?
NO then diffuses through endothelial cells to smooth muscle cells —> inc cGMP —> ATPase that pumps Ca++ out (RELAX)
How do myogenic autoregulation and sheer force work against ea other?
- Oppose one another to keep ea other in check
- Inc pressure —> dec radius to maintain flow (vasoconstriction)
- Sheer stress —> NO production —> relaxation (vasodilation)
- Further… decrease radius in myogenic regulation —> greater sheer stress b/c more drag along vessel wall —> vasodilation that directly counteracts myogenic regulation
Coronary Muscle Circulation
- Coronary capillary blood flow is pulsatile (while blood flow is usually constant by the time it gets to all other capillaries); falls during systole b/c ventricular contraction compressed capillaries; rise in diastole as compression removed
Cerebral Circulation
- KEEP CONSTANT FLOW
* But regional changes in blood flow; certain pats of brain can get more flow if inc CO2 (vasodilation)
Skeletal Muscle Circulation
- Epi binds beta receptors —> vasodilation BUT not all skeletal muscle vascular beds can be dilated b/c HUGE contribution to TPR esp if dec BP in exercise
- SO…local factors (paracrine) ensure vasodilation of only working muscle
- If hemorrhage … enough epi to work on alpha as well so vasoconstriction instead
GI Circulation
Inc gut blood flow during digestion —> dec flow to other parts of body (“post-prandial hypotension”)
Cutaneous Circulation
- Dep more on temp than BP
- When body if overheated —> inc blood flow to skin to cool it
- Bradykinin released when sweating —> NO —> vasodilation to inc flow to skin for cooling
- When body is cold —> dec blood flow to skin to keep warm
Bradykinin
Released when sweating and released from damaged endothelial cells
Both results in vasodilation
Pulmonary Circulation
- ALL THESE PRINCIPLE DO NOT APPLY TO PULM CIRC
* Goal = oxygenate blood so shunt blood to high pO2 not low pO2
