Vascular Control Flashcards
Preferential Channel
Larger capillary not separated by sphincter, so blood flows from metarteriole through here at rest
Pericytes Central vs. Peripheral
Essential part of BBB w/ contractile action vs. stem cells
Importance of Endothelial -> SM Gap Junction
Transfers hyperpolarizing factor from endo -> SM
Activation of Smooth Muscle
Ca-calmodulin activates MLCK, leading to P-Myosin and contraction
2 Mechs to get Ca for Contraction
Electromechanical coupling -> CICR and RyR
Chemomechanical Coupling -> NE activating alpha1 -> IP3R
3 Pathways for Beta2 Inhibition of Contraction
cAMP activates K+ channels leading to hyperpol
PKA releases just enough Ca from SR to activate Na-Ca exchanger and extrude Ca
Blocks IP3R
CGRP
Something that activates Beta2s and causes vascular relaxation
Epi Concentration and Vasodilation/Constriction Results
Low = dilator high = constrictor
2 Locations of Parasympathetic bv Effect
Heart (SA Node/Atria)
External Genitalia
Dual Innervation of Skeletal Muscle Arterioles
From symp, NE but also ACh acting on MRs on endothelial cells
IV Infusion of Epi (CO, PVR, and ABP [sys, mean, dias], and Rs for 1st 2)
CO increase via Beta1s
PVR decrease via Beta2s
So systolic increase, dystolic decrease in BP, and mean relatively constant
IV Infusion of NE (CO, PVR, and ABP and explanation)
No effect (require higher conc, like NE released from synapse)
Increase via alpha1s
All 3 increase (sys, mean, dias)
Angiotensin II (production and 4 targets for effects)
Produced by ACE in lungs from AT1 from low BP. Acts on hypothal to increase thirst, adrenal cortex to release aldosterone, renal prox tubules to decrease Na excretion, and peripheral arterioles to increase SVR, all increasing bv and arterial pressure
2 HTN Treatments Related to ATII
ACE inhibitors or ATII R inhibitors, bc most HTN not at renal origin
2 Hypotheses for Local Regulation
Vasodilator Hypothesis: Metabolites from tissue use causes vasodilation, and are then washed away proportional to blood flow
Oxygen Demand Hypothesis: Smooth muscle requires O2, so high O2 means sphincters contracted and low means open. Simplistic
Active vs. Reactive Hyperemia
Increased blood flow caused by activity of tissue vs. transient increase due to temporary deprivation (metabolites accumulate)
2 Sources of ATP Release
Endothelial cells in response to shear stress
Erythrocytes from shear stress or low O2 content
Oxygen Delivery Pathway of ATP
Ecytes release ATP when sense low O2. Activates ATP-induced ATP release Rs on ecytes and endothelial cells via IC Ca from IP3 activation. So signal propagates but also activates eNOS in endothelials to produce NO and relax smooth muscle. So more blood/O2 comes in acting as own neg feedback
Pannexins
Modified gap junction prots that now in verts just act as ATP release channels. Who gives a damn about all that evolutionary bullshit these professors seem to jizz to
Autoregulatory Range
Tissue-specific range of arterial pressure in which a change will cause only a transient change in blood flow and then resettlement to a similar steady-state.
2 Theories of Autoregulation of Blood Flow
Metabolic Theory - Flow washes out vasodilator substances
Myogenic Theory - stretch sensitivity of smooth muscle
3 Locations of Mainly Metabolic Control and 3 of Mainly Nerval Control
Heart, skeletal muscle, brain
Kidneys, skin, splanchnic organs
Coronary Blood Flow Metabolic and Neural Control
Adenosine from myocardial cells vs. beta2s stimulated by symp resulting in relaxation
Difference in L and R Coronary Blood Flow
Highest pressure from LV causes L coronary flow to decrease and even retrograde. R Coronary decreases but maintains continuous perfusion
