Pressure and Flow Control Flashcards

1
Q

Primary source of nitric oxide

A

endothelium

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2
Q

Intrinsic Mechanism

A

Local control
Often does not affect systemic blood pressure; only affects local mechs
Autoregulation - tissues can control their own blood flow to meet their metabolic needs

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3
Q

Extrinsic Control

A

Autonomic NS and circulating hormones regulate BP

Essential driving force for blood flow and redistribution

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4
Q

Mechanisms involved in autoregulation (keeping flow constant)

A
  1. Myogenic - smooth muscle
  2. Metabolic
  3. Paracrine - substances released locally
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5
Q

How does flow stay constant

A

Changing resistance

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6
Q

MEtabolic Autoregulation

A

Matching flow with tissue metabolic activity
Metabolites = local vasodilation
Inc them, inc blood flow to wash out the metabolites
Then blood flow will decrease until metabolites accumulate again

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7
Q

Hyperemia

A

Increase in flow

  1. Active - dilation in response to inc metabolic activity (exercise)
  2. Reactive - increase in accumulation of vasodilator metabolites due to occlusion (happens every single beat - BP cuff)
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8
Q

Myogenic Autoregulation

A

Inc transmural pressure causes smooth muscle vasoconstriction
Activation of stretch will activate the stretch activated channels on the VSM
This induces depolarization and Ca influx

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9
Q

Decrease in transmural pressure would cause smooth muscle ____

A

dilation

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10
Q

Inc in arterial and transmural pressure —>

A

Stretch of smooth muscle –> contraction of the muscle –> arteriolar constriction –> dec in blood flow

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11
Q

Paracrine Mechanism - major dilators

A

Nitric Oxide
Prostacyclin
EDHF

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12
Q

Paracrine Mechanism - major constrictors

A

Angiotensin II
Thromboxane A2
Endothelium

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13
Q

Metabolic - dilate or constrict

A

Vasodilator

metabolites

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14
Q

Myogenic Control - dilate or constrict

A

Can do either
Depends on the stress
Inc pressure = constrict
Dec pressure = dilate

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15
Q

Paracrine - shear stress will cause

A

NO release from endothelium

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16
Q

Paracrine Dilators

A

Relax

  1. NO
  2. Prostacyclin
  3. EDHF
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17
Q

Paracrine Relaxer - NO

A

Ach stimulates NO release
NO is produced from reaction with L-Arg (amino acid) and NOS (nitric oxide synthase - synthesizes NO)
NO then uses cGMP to produce relaxation

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18
Q

Paracrine Relaxer - Prostacyclin

A

From arachadonic acid

Inc cAMP to cause relaxation

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19
Q

Paracrine Relaxer - EDHF

A

Endothelium derived hyperpolarized factor

Takes membrane potential further away from potential by allowing K to leave the cell and therefore relax

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20
Q

What happens prior to symptoms of cardiovascular disease

A

Endothelial dysfunction

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21
Q

Key underlying Mechanisms - Endothelial Dysfunction

A
  1. Arginase also competes for L arg (like NO)
    if arg is elevated will produce less NO
  2. Could have less L-Arg around - so less NO
  3. Missing BH4 - get superoxide - free radical - oxidative stress
  4. Elevation of Rho Kinase - leads to dec in NO by inhibiting myosn light chain phosphokinase and keeps myosin in contracted state
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22
Q

Risk factors for cardiovascular disease

A
Hypertension
Hypercholesterolemia
Diabetes Mellitus
Aging
Obesity
Smoking
Meopause
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23
Q

What do risk factors of cardiovascular disease all have in common?

A

They all lead to oxidative stress –> endothelial dysfunction and therefore cardiovascular dysfunction

24
Q

Extrinsic Control

A

Neural/Hormonal
Sympathetic = NE and adrenergic receptors
Parasympathetic = Ach and cholinergic receptors

25
Q

Extrinsic - Sympathetic

A

Alpha adrenergic receptors = dense in vasculature, more sparse in heart, cause VC
Bete adrenergic = dense in heart, more sparse in vasculature, cause inc in HR and contractility and VD in vasculature

26
Q

Extrinsic - Parasympathetic

A

Ach –> cholinergic receptors (muscarinic and nicotinic)
Limited innervation of vasculature
Reduces HR
Extremely limited to erectile tissue

27
Q

With exercise what happens to flow and why?

A

Inc blood flow

SNA will inc resistance

28
Q

MAP =

A

CO x TPR

29
Q

Short Term Regulation of BP

A
Baroreceptors - beat to beat regulation 
Baroreflex is a pressure-lowering mechanism
- Detects change in pressure
- goes to center in medulla
- effector = SNS to change BP
30
Q

Long Term Regulation of BP

A
Pressure/volume receptors in kidneys adjust 
RAA system (Renin angiotensin aldosterone)
31
Q

High Pressure Receptors location

A

Aortic arch and carotid sinus

32
Q

Low Pressure Receptros location

A

AKA Cardiopulmonary Receptors
All chambers of the heart and great veins
As filling, pressure goes down and stimulates an increase in vasoconstriction

33
Q

Cardiovascular Control Center =

A

Medulla

Afferent fibers project to medulla; specifically nucleus tractus solitarius (NTS)

34
Q

Nucleus Tractus Solitarius receives inputs from

A

Respiratory Centers

Higher CNS center (emotion)

35
Q

Baroreflex stimulates

A

Inhibitory interneurons project from NTS to vasomotor area

Excitatory interneurons project from NTS to coinhibitory area - stimulates parasympathetic vagus nerve

36
Q

Drop in arterial pressure - what comes to rescue?

Get up too fast

A
Baroreflex
There is a dec in baroreflex activity 
Inc symp nerve activity 
inc HR, contractility, vascular resistance, vasoconstriction 
BP will go up back to set point
37
Q

Inc in arterial pressure - then what

A

Inc baroreceptor activity
Vagus responds and dec HR and dec CO and pressure will go down
Sleeper effect when in choke hold

38
Q

Small drop in pressure will elicit what kind of change

A

A huge change

39
Q

Make card on beat to beat regulation

A

As you dec. pressure you are inc sympathetic activity

Sympathetic nerve activity happens primarily during diastole

40
Q

If you inc sympathetic nerve activity what tissues/organs are impacted most

A

Skin muscle and kidney are affected the most

Brain and heart are not impacted because to keep things constant we dont want to take away from the brain and heart

41
Q

What will win with competition for flow?

A

Heart and brain

42
Q

Reduced slope of the barorector curve means

A

Reduced gain or sensitivity - means baroreflex opposition to changes in BP would be reduced
Gain is reduced with most CV pathologies

43
Q

Baroreflex is ____ to defend a new set point

A

Reset

When we increase intensity of exercise, we are shifting the set point

44
Q

How does the resetting occur?

A

Central Command

Exercise Pressor Reflex

45
Q

Central Common control of resetting

A

Feed forward mechanism
Central Command = feedforward control
If inc. output from motor cortex, then inc CC, and this results in inc sympathetic nerve activity

46
Q

Exercise Pressor Reflex - resetting

A

= mechanoreflex and metaboreflex

If inc in metabolites and/or contraction in active muscle, Inc in sympathetic nerve activity

47
Q

Greater motor output will do what to setpoint

A

Reset it

As metabolites build up - will also reset it

48
Q

Long Term BP Regulation

A

Juxtaglomerular Apparatus

49
Q

3 Cell types of JG Apparatus

A
  1. Granular Cells - release renin
  2. Macula Densa Cells - senses filtered Na load
  3. Extraglomerular mesangial cells
50
Q

Renin Angiotensin Aldosterone System

A

JGA –> releases renin –> (renin converts angiotensinogen to angiotensin I –> converting enzyme in lungs converts angiotensin I to angiotensin II –> causes constrictor effect that will inc pressure –> acts on adrenal cortex and stimulates production of aldosterone (Na conserving hormone)
Inc volume, so pressure will go back up

51
Q

Stimulus of drop in pressure/volume

A

Dec renal arterial pressure –> inc renin secretion

Will also activate baroreceptor reflex –> inc in sympathetic nerve activity –> inc in renin secretion

52
Q

When renin is elevated, then what

A

Will produce Angiotensin II –> Vasoconstriction –> Inc peripheral resistance = inc BP

53
Q

WHat 3 mechanisms aid in ncreasing renin secretion

A

Inc renal sympathetic nerve activity
Decrease in Macula Densa NaCl load
Renal Baroreceptor

54
Q

What leads to vasoconstriction

A

Exercise pressure reflex
Central Command
Baroreflex
Myogenic

55
Q

What leads to vasodilation

A

Metabolic autoregulation
Nitric oxide
Muscle pump
- these win during exercise - they outweigh the VC mechanisms so VD will occur