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FS Exam 4 > Pressure and Flow Control > Flashcards

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
Extrinsic - Sympathetic
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
Extrinsic - Parasympathetic
Ach --> cholinergic receptors (muscarinic and nicotinic) Limited innervation of vasculature Reduces HR Extremely limited to erectile tissue
27
With exercise what happens to flow and why?
Inc blood flow | SNA will inc resistance
28
MAP =
CO x TPR
29
Short Term Regulation of BP
``` 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
Long Term Regulation of BP
``` Pressure/volume receptors in kidneys adjust RAA system (Renin angiotensin aldosterone) ```
31
High Pressure Receptors location
Aortic arch and carotid sinus
32
Low Pressure Receptros location
AKA Cardiopulmonary Receptors All chambers of the heart and great veins As filling, pressure goes down and stimulates an increase in vasoconstriction
33
Cardiovascular Control Center =
Medulla | Afferent fibers project to medulla; specifically nucleus tractus solitarius (NTS)
34
Nucleus Tractus Solitarius receives inputs from
Respiratory Centers | Higher CNS center (emotion)
35
Baroreflex stimulates
Inhibitory interneurons project from NTS to vasomotor area | Excitatory interneurons project from NTS to coinhibitory area - stimulates parasympathetic vagus nerve
36
Drop in arterial pressure - what comes to rescue? | Get up too fast
``` 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
Inc in arterial pressure - then what
Inc baroreceptor activity Vagus responds and dec HR and dec CO and pressure will go down Sleeper effect when in choke hold
38
Small drop in pressure will elicit what kind of change
A huge change
39
Make card on beat to beat regulation
As you dec. pressure you are inc sympathetic activity | Sympathetic nerve activity happens primarily during diastole
40
If you inc sympathetic nerve activity what tissues/organs are impacted most
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
What will win with competition for flow?
Heart and brain
42
Reduced slope of the barorector curve means
Reduced gain or sensitivity - means baroreflex opposition to changes in BP would be reduced Gain is reduced with most CV pathologies
43
Baroreflex is ____ to defend a new set point
Reset | When we increase intensity of exercise, we are shifting the set point
44
How does the resetting occur?
Central Command | Exercise Pressor Reflex
45
Central Common control of resetting
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
Exercise Pressor Reflex - resetting
= mechanoreflex and metaboreflex | If inc in metabolites and/or contraction in active muscle, Inc in sympathetic nerve activity
47
Greater motor output will do what to setpoint
Reset it | As metabolites build up - will also reset it
48
Long Term BP Regulation
Juxtaglomerular Apparatus
49
3 Cell types of JG Apparatus
1. Granular Cells - release renin 2. Macula Densa Cells - senses filtered Na load 3. Extraglomerular mesangial cells
50
Renin Angiotensin Aldosterone System
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
Stimulus of drop in pressure/volume
Dec renal arterial pressure --> inc renin secretion | Will also activate baroreceptor reflex --> inc in sympathetic nerve activity --> inc in renin secretion
52
When renin is elevated, then what
Will produce Angiotensin II --> Vasoconstriction --> Inc peripheral resistance = inc BP
53
WHat 3 mechanisms aid in ncreasing renin secretion
Inc renal sympathetic nerve activity Decrease in Macula Densa NaCl load Renal Baroreceptor
54
What leads to vasoconstriction
Exercise pressure reflex Central Command Baroreflex Myogenic
55
What leads to vasodilation
Metabolic autoregulation Nitric oxide Muscle pump - these win during exercise - they outweigh the VC mechanisms so VD will occur

FS Exam 4 (6 decks)

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