05c: Regulation Flashcards by Nuna H

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?

X = flow
Y = arteriolar resistance

Myogenic response (autoregulation)

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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.

Depolarizing;
Increase
Frequency

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

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

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

Decrease; decrease; increase

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

False - not to same extend in every vascular bed

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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.

Increase;
K concentration
Too many;
Increase

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

X = skeletal

Vasodilator

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The vasodilation of resistance vessels depends on which three mechanisms?

Hyperpolarization
Reduced Ca mobilization
Inactivation of myosin LC kinase

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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).

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

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

X = increase in extra cellular K conc
Hyperpolarization
Relaxation

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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?

Positive;
Raised
Hyperpolarization (K leaves)

Vm of cell oscillates sufficiently above Ek

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

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

Shear stress

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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?

Decrease;
X = NO

Decrease Ca conductance channel activity
Increase ATPase activity to resequester Ca

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

Adenosine binds receptor (leads to activation of adenylyl cyclase)
Production of cAMP increased
Activation of PKA
PKA phosphorylates and inhibits MLCK

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

X = sympathetic division of ANS

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

X = NE
Y = alpha-1

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

False - opposite

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

True

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

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

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

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

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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?

X = NE
Y = alpha-1
Increase;

Raises it - shifts blood to arterial side

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

Parasympathetic NS Doesn’t regulate venous tone

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

Both

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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?

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

NE
Z = Beta-1

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

All chambers; SA/AV nodes and atria most densely innervated

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

``` X = R vagus Y= L vagus ```

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

All chambers; SA and AV nodes highest density

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

Both

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

Vagal

Where, specifically, is the "CV Control Center"?

Medulla and lower pons

(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.

X = rostral ventrolateral medulla Excitatory Preganglionics

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

Pre-ganglionics Tonically; Inhibited X = raphe nucleus

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).

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

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

``` X = nucleus ambiguus and dorsal motor nucleus X Y = vagus nerve ```

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

Inhibited; | X = caudal ventrolateral medulla

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

``` X = carotid sinuses (glossopharyngeal) Y = aortic arch (vagus) ```

T/F: baroreceptors are stretch receptors.

True

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

False - increase firing frequency in response to this

Baroreceptor afferents respond to changes in:

1. Instantaneous P 2. Rate of change of P 3. Pulse P

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

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

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

X = mean aortic BP | sinus

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

X = nucleus of solitary tract Activate 1. Cardioinhibitory center 2. Depressor areas

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

Greater (more than half flows out in first half of runoff time) More volume = more pressure = greater driving force for flow

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

X = contractility

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

Increase (higher diastolic P in aorta/reservoir); Decrease (decrease SV)

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

Decrease; | Decrease

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

Increase; increase

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

Increase (due to increase in diastolic P); increase

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

``` Decrease; decreasing EDV (less time for runoff ``` Increases CO Ex: (120 bpm)*(over 50 mL) is greater value than (60 bpm)*(100 mL)

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).

Increase; | HR (SV likely decreased)

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

Non-myelinated; | X = vagal

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

Relaxation; Inhibiting; Myosin crossbridge

Which molecule plays role in regulatory parasympathetic vasodilation?

There is NO regulatory parasympathetic vasodilation

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

Less (less compliant)

Contractility is predominantly regulated by:

Increases/decreases in sympathetic activity

"Central venous pressure" refers to P in:

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

``` 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)

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).

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

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

X = forearm; 1. Increase driving force and/or 2. Decrease resistance

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

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

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

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

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

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

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

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

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

contraction

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

relaxation

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

``` X = skeletal muscle Y = Epi Z = dose ```

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

Beta-2; | Vasodilation

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

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

Renin action.

Cleaves angiotensinogen to angiotensin I

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

``` X = renin cleavage of angiotensinogen Y = ACE (angiotensin converting enzyme) Z = angiotensin II ```

Where could you find ACE (angiotensin converting enzyme)?

1. Lumenal surface of capillary endothelium | 2. Plasma

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

II; vasoconstrictor

List the key 6 actions of Angiotensin II.

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

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

Promotes; X = adrenal cortex Promotes renal Na retention

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

Promotes; X = posterior pituitary Promotes renal H2O retention

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

X = hypothalamic receptors | Increase

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

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

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

X = atrial natriuretic peptide (ANP)

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

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