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05c: Regulation Flashcards

1
Q

The near constant (X), in face of rise/fall in perfusion pressure of pre-capillary vessels, results from increase/decrease in (Y). What type of regulation is this?

A 
X = flow
Y = arteriolar resistance

Myogenic response (autoregulation)

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2
Q

In myogenic response, factors that increase contractile response by (de/re/hyper)-polarizing membrane do so by (increasing/decreasing) (time/frequency/amplitude) of spike discharge.

A

Depolarizing;
Increase
Frequency

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3
Q

Stretch-sensitive cationic channels play role in (X) response/regulation. With (increase/decrease) (Y), they distend and promote (Z).

A

X = autoregulation/myogenic response
Increase;
Y = perfusion P
Z = depolarization, increase frequency of AP and contractile activity of smooth muscle

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4
Q

An (increase/decrease) in PO2 and (increase/decrease) in pH and (increase/decrease) in PCO2 all contribute to decrease resistance in vascular smooth muscle.

A

Decrease; decrease; increase

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5
Q

T/F: during exercise, resistance is lowered to same extend in vascular smooth muscle beds.

A

False - not to same extend in every vascular bed

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6
Q

During exercise, (Increase/decrease) in (X), resulting from (too few/many) skeletal muscle AP potentials, as well as (increase/decrease) in osmolality will reduce arteriolar tension.

A

Increase;
K concentration
Too many;
Increase

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7
Q

In heart and (X), muscle, adenosine is an effective (vasodilator/vasoconstrictor).

A

X = skeletal

Vasodilator

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8
Q

The vasodilation of resistance vessels depends on which three mechanisms?

A
  1. Hyperpolarization
  2. Reduced Ca mobilization
  3. Inactivation of myosin LC kinase
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9
Q

K-ATP channels are typically (open/closed) when (X) is bound. But in (increase/decrease) of (Y), such as during exercise, they (open/close) and allow (de/hyper)-polarization, causing smooth muscle to (contract/relax).

A

Closed
X = ATP
Decrease ATP (or low Po2/pH, high PCO2)
Open; hyperpolarization; relaxation

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10
Q

K-IR channels open in response to (X), causing (de/hyper)-polarization of cell and (contraction/relaxation) of arteriolar smooth muscle.

A

X = increase in extra cellular K conc
Hyperpolarization
Relaxation

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11
Q

Despite the slight shift of Ek toward more (positive/negative) value when K conc is (lowered/raised) extracellularly, opening of K-IR channels in vascular smooth muscle still causes (de/hyper)-polarization. Why?

A

Positive;
Raised
Hyperpolarization (K leaves)

Vm of cell oscillates sufficiently above Ek

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12
Q

NO is produced as result of (hypo/hyper)-capnia, aka (X) and activates (Y) channels. Which other situation can produce NO?

A

Hypercapnia;
X = increase PCO2
Y = “big conductance” K channels

Shear stress

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13
Q

Vasodilation of arteriolar smooth muscle via (increase/decrease) in Ca conductance is mediated by (X) molecule. The signaling cascade impacts activity of which channels/molecules?

A

Decrease;
X = NO

  1. Decrease Ca conductance channel activity
  2. Increase ATPase activity to resequester Ca
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14
Q

List steps leading to (relaxation/constriction) of vascular smooth muscle via inactivation of myosin LC kinase.

A
  1. Adenosine binds receptor (leads to activation of adenylyl cyclase)
  2. Production of cAMP increased
  3. Activation of PKA
  4. PKA phosphorylates and inhibits MLCK
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15
Q

(X) nervous system is the primary regulator for TPR.

A

X = sympathetic division of ANS

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16
Q

TOR: (X) released from sympathetic nerve endings, binds to its (Y) receptor and stimulates contraction of vascular smooth muscle.

A 
X = NE
Y = alpha-1
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17
Q

T/F: large arteries are more richly innovated with post-ganglionic adrenergic fibers, compared with smaller arteries and arterioles.

A

False - opposite

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18
Q

T/F: skin is more richly innovated with post-ganglionic adrenergic fibers, compared with the brain.

A

True

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19
Q

Under basal conditions, the degree of “tone” in resistance vessels is maintained by (autoregulation/sympathetics).

A

Both - vasoconstrictor fibers contribute low-level stimulation (1-3 impulses/sec)

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20
Q

T/F: extrinsic control of vascular bed resistance via adrenergic nerves is done by initiation of AP.

A

False - via increase or decrease in impulse frequency (compared to low-level basal condition)

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21
Q

Adrenergic nerves release (X) to bind (Y) receptors on veins and some venules. This causes (increase/decrease) in venous tension, which subsequently has which effect on arterial BP?

A

X = NE
Y = alpha-1
Increase;

Raises it - shifts blood to arterial side

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22
Q

Parasympathetic NS regulates venous tone by releasing (X) to bind to its (Y) receptor.

A

Parasympathetic NS Doesn’t regulate venous tone

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23
Q

Cardiac function is regulated by (parasympathetic/sympathetic) NS.

A

Both

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24
Q

Sympathetic innervation to heart: pre-gang arise from (X) and synapse on ganglia that give rise to (Y) nerves. Which transmitter is used, binding to its (Z) receptor?

A 
X = T1-5
Y = superior, middle, inferior cardiac

NE
Z = Beta-1

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25
Q

Which chambers of heart innervated by sympathetic NS? List the locations with richest supply.

A

All chambers;

SA/AV nodes and atria most densely innervated

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26
Q

Parasympathetic innervation to heart: (X) nerve to SA node and (Y) nerve to AV node.

A 
X = R vagus
Y= L vagus
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27
Q

Which chambers of heart innervated by parasympathetic NS? List the locations with richest supply.

A

All chambers;

SA and AV nodes highest density

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28
Q

(Vagal/sympathetic) nerves to heart are tonically active.

A

Both

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29
Q

At rest, (Vagal/sympathetic) innervation to heart predominates.

A

Vagal

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30
Q

Where, specifically, is the “CV Control Center”?

A

Medulla and lower pons

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31
Q

(X) houses the “pressor” area of the CV Control Center. These neurons are spontaneously active and have (excitatory/inhibitory) effect on (pre/post)-ganglionic sympathetics.

A

X = rostral ventrolateral medulla
Excitatory
Preganglionics

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32
Q

CV control center: SC sympathetic (pre/post)-ganglionics are (tonically/spontaneously) (stimulated/inhibited) by depressor areas in (X) location.

A

Pre-ganglionics
Tonically;
Inhibited

X = raphe nucleus

33
Q

CV control center: the net effect of the antagonistic pressor/depressor activity on (X) is (excitatory/inhibitory). Thus, under resting conditions, (X) are (silenced/activated).

A 
X = sympathetic pre-ganglionics (SC)
Excitatory;
Mildly activated (hence basal 1-3 impulses/sec)
34
Q

Parasympathetics of CV control center have cell bodies in (X) and preganglionic axons travel in (Y).

A 
X = nucleus ambiguus and dorsal motor nucleus X
Y = vagus nerve
35
Q

CV control center: Pressor area of CV control center is tonically (activated/inhibited) by (X) depressor area under rest conditions.

A

Inhibited;

X = caudal ventrolateral medulla

36
Q

Arterial baroreceptors are concentrated in (X) and (Y) locations. Adherents from each location travel via which nerves?

A 
X = carotid sinuses (glossopharyngeal)
Y = aortic arch (vagus)
37
Q

T/F: baroreceptors are stretch receptors.

38
Q

T/F: baroreceptor afferents start firing in response to rise in blood pressure, thus distension of artery.

A

False - increase firing frequency in response to this

39
Q

Baroreceptor afferents respond to changes in:

A
  1. Instantaneous P
  2. Rate of change of P
  3. Pulse P
40
Q

T/F: as long as mean arterial BP is being maintained, baroreceptors are happy.

A

False - will respond to low pulse pressure, even of mean arterial BP is maintained

41
Q

The threshold (X) for firing of (sinus/aortic) baroreceptor afferents is lower.

A

X = mean aortic BP

sinus

42
Q

Arterial baroreceptor sensory fibers form synapses in (X) nucleus. (X) has neurons that (activate/inhibit) which CV control areas?

A

X = nucleus of solitary tract

Activate

  1. Cardioinhibitory center
  2. Depressor areas
43
Q

CV model: in the reservoir, runoff is (less/equal/greater) in first half of the time. Why?

A

Greater (more than half flows out in first half of runoff time)

More volume = more pressure = greater driving force for flow

44
Q

Put simply, without a change in (X), the heart pumps what it gets.

A

X = contractility

45
Q

Increase TPR will (increase/decrease) MAP and (increase/decrease) CO.

A

Increase (higher diastolic P in aorta/reservoir);

Decrease (decrease SV)

46
Q

Increase Cv (venous compliance) will (increase/decrease) MAP and (increase/decrease) CO.

A

Decrease;

Decrease

47
Q

Increase contractility will (increase/decrease) MAP and (increase/decrease) CO.

A

Increase; increase

48
Q

Increase HR will (increase/decrease) MAP and (increase/decrease) CO.

A

Increase (due to increase in diastolic P); increase

49
Q

Increase HR will (increase/decrease) SV by (increasing/decreasing) (EDV/ESV). How does this affect CO?

A 
Decrease;
decreasing EDV (less time for runoff

Increases CO
Ex: (120 bpm)(over 50 mL) is greater value than (60 bpm)(100 mL)

50
Q

Athlete experiences increase in HR while working out. It’s likely that his (increase/decrease) in CO is due to the increase in (HR/SV/both).

A

Increase;

HR (SV likely decreased)

51
Q

Stretch receptors associated with (myelinated/non-myelinated) (X) sensory nerve fibers contribute feed-forward cardiopulmonary reflex.

A

Non-myelinated;

X = vagal

52
Q

It’s thought that adenosine causes smooth muscle (contraction/relaxation) by (stimulating/inhibiting) (X).

A

Relaxation;
Inhibiting;
Myosin crossbridge

53
Q

Which molecule plays role in regulatory parasympathetic vasodilation?

A

There is NO regulatory parasympathetic vasodilation

54
Q

NE effect: vein will have (less/greater) volume for any given transmural pressure.

A

Less (less compliant)

55
Q

Contractility is predominantly regulated by:

A

Increases/decreases in sympathetic activity

56
Q

“Central venous pressure” refers to P in:

57
Q

Feedforward reflex: you raise your legs while lying down, causing increase in (X) P, but no increase in (Y) P. Explain.

A 
X = central venous (RA) pressure (due to increase VR)
Y = arterial pressure

Increase blood flow to arms (adjustment made via decreasing resistance in arms to maintain BP)

58
Q

Feedforward reflex: you raise your legs while lying down, causing (increase/decrease) in VR. This is due to (increase/decrease) in vein P, specifically compared to (X).

A

Increase;
Decrease;
X = atmospheric P (compresses veins)

59
Q

Feedforward reflex: you raise your legs while lying down, causing increase in flow to (X). What is this attributed to?

A

X = forearm;

  1. Increase driving force and/or
  2. Decrease resistance
60
Q

Epi is released from (X) cells following stimulation by (Y). List some scenarios that would cause Epi release.

A 
X = adrenal medulla (chromaffin cells)
Y = preganglionic sympathetic fibers
  1. Low BP
  2. Exercise
  3. Fight/flight
61
Q

Epi binds to (X) receptors on heart and causes (increase/decrease) in (Y).

A

X = beta-1
Increase;
Y = HR and contractility

62
Q

Epi binds to (X) receptors on veins and causes (increase/decrease) in (Y).

A

X = alpha-1;
Increase;
Y = venous smooth muscle tone

63
Q

Epi has variable effect on (venous/arteriolar) smooth muscle due to:

A

Arteriolar;

two calsses of receptors (alpha-1 and beta-2)

64
Q

Epi binding to alpha-1 receptor on arteriolar muscle causes:

A

contraction

65
Q

Epi binding to beta-2 receptor on arteriolar muscle causes:

A

relaxation

66
Q

In structures, such as (X), with both alpha-1 and beta-2 (Y) receptors, the response is (Z)-dependent.

A 
X = skeletal muscle
Y = Epi
Z = dose
67
Q

Under low Epi conditions, (alpha/beta) (1/2) receptor binds it with higher affinity, causing (vasoconstriction/vasodilation).

A

Beta-2;

Vasodilation

68
Q

Renin is a(n) (X) that is predominantly synthesized by (Y) cells. What triggers its release?

A 
X = protease
Y = juxtaglomerular cells (of kidney)
  1. Local decrease in renal perfusion P
  2. Sympathetic nerve activation
69
Q

Renin action.

A

Cleaves angiotensinogen to angiotensin I

70
Q

Angiotensin I is formed by (X) and acted on by (Y) to produce (Z).

A 
X = renin cleavage of angiotensinogen
Y = ACE (angiotensin converting enzyme)
Z = angiotensin II
71
Q

Where could you find ACE (angiotensin converting enzyme)?

A
  1. Lumenal surface of capillary endothelium

2. Plasma

72
Q

Angiotensin (I/II) is potent (vasoconstrictor/vasodilator).

A

II; vasoconstrictor

73
Q

List the key 6 actions of Angiotensin II.

A
  1. Vasoconstricts arterioles
  2. Facilitates NE release
  3. Stimulates Pressor area
  4. Triggers aldosterone release
  5. Stimulates thirst
  6. Stimulates ADH release
74
Q

Angiotensin II (promotes/inhibits) release of aldosterone from (X). This has which effect?

A

Promotes;
X = adrenal cortex

Promotes renal Na retention

75
Q

Angiotensin II (promotes/inhibits) release of ADH from (X). This has which effect?

A

Promotes;
X = posterior pituitary

Promotes renal H2O retention

76
Q

Interaction of angiotensin II with (X) leads to (increase/decrease) sensation of thirst.

A

X = hypothalamic receptors

Increase

77
Q

At high concentrations, ADH has (vasoconstrictor/vasodilator) effect via (X) receptors. The exception is in (Y) locations, which have (Z) receptors.

A

Vasoconstrictor (thus, vasopressin);
X = V2
Y = heart and brain
Z = V1

78
Q

(X), synthesized and secreted primarily by modified myocytes in atria, acts in opposition of angiotensin II.

A

X = atrial natriuretic peptide (ANP)

79
Q

List the key 6 actions of ANP (atrial natriuretic peptide).

A
  1. Blocks ACh release from pregang symp
  2. Inhibits synthesis of alpha-1 receptors
  3. Inhibits renin synthesis
  4. Inhibits Pressor area
  5. Inhibits aldosterone secretion
  6. Inhibits renal Na retention

CVS (11 decks)

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