Vascular Control Flashcards

1
Q

Preferential Channel

A

Larger capillary not separated by sphincter, so blood flows from metarteriole through here at rest

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2
Q

Pericytes Central vs. Peripheral

A

Essential part of BBB w/ contractile action vs. stem cells

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3
Q

Importance of Endothelial -> SM Gap Junction

A

Transfers hyperpolarizing factor from endo -> SM

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4
Q

Activation of Smooth Muscle

A

Ca-calmodulin activates MLCK, leading to P-Myosin and contraction

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5
Q

2 Mechs to get Ca for Contraction

A

Electromechanical coupling -> CICR and RyR

Chemomechanical Coupling -> NE activating alpha1 -> IP3R

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6
Q

3 Pathways for Beta2 Inhibition of Contraction

A

cAMP activates K+ channels leading to hyperpol
PKA releases just enough Ca from SR to activate Na-Ca exchanger and extrude Ca
Blocks IP3R

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7
Q

CGRP

A

Something that activates Beta2s and causes vascular relaxation

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8
Q

Epi Concentration and Vasodilation/Constriction Results

A

Low = dilator high = constrictor

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9
Q

2 Locations of Parasympathetic bv Effect

A

Heart (SA Node/Atria)

External Genitalia

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10
Q

Dual Innervation of Skeletal Muscle Arterioles

A

From symp, NE but also ACh acting on MRs on endothelial cells

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11
Q

IV Infusion of Epi (CO, PVR, and ABP [sys, mean, dias], and Rs for 1st 2)

A

CO increase via Beta1s
PVR decrease via Beta2s
So systolic increase, dystolic decrease in BP, and mean relatively constant

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12
Q

IV Infusion of NE (CO, PVR, and ABP and explanation)

A

No effect (require higher conc, like NE released from synapse)
Increase via alpha1s
All 3 increase (sys, mean, dias)

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13
Q

Angiotensin II (production and 4 targets for effects)

A

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

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14
Q

2 HTN Treatments Related to ATII

A

ACE inhibitors or ATII R inhibitors, bc most HTN not at renal origin

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15
Q

2 Hypotheses for Local Regulation

A

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

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16
Q

Active vs. Reactive Hyperemia

A

Increased blood flow caused by activity of tissue vs. transient increase due to temporary deprivation (metabolites accumulate)

17
Q

2 Sources of ATP Release

A

Endothelial cells in response to shear stress

Erythrocytes from shear stress or low O2 content

18
Q

Oxygen Delivery Pathway of ATP

A

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

19
Q

Pannexins

A

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

20
Q

Autoregulatory Range

A

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.

21
Q

2 Theories of Autoregulation of Blood Flow

A

Metabolic Theory - Flow washes out vasodilator substances

Myogenic Theory - stretch sensitivity of smooth muscle

22
Q

3 Locations of Mainly Metabolic Control and 3 of Mainly Nerval Control

A

Heart, skeletal muscle, brain

Kidneys, skin, splanchnic organs

23
Q

Coronary Blood Flow Metabolic and Neural Control

A

Adenosine from myocardial cells vs. beta2s stimulated by symp resulting in relaxation

24
Q

Difference in L and R Coronary Blood Flow

A

Highest pressure from LV causes L coronary flow to decrease and even retrograde. R Coronary decreases but maintains continuous perfusion

25
Q

3 Aspects of Skeletal Blood Flow Control

A

Metabolic control relaxes arterioles
Collateral vasoconstriction in nonreactive part of muscle to shift blood w/in muscle
Cholinergic Symp Fibers onto endothelials stimulate eNOS for relaxation

26
Q

Kidney Decrease in Blood Flow

A

Cont’d Maximal effort decreases blood flow, so can get kidney failure in marathons and shit

27
Q

Bayliss Effect

A

Pronounced autoregulation in isolated (denervated) kidney. Mainly myogenic