Circulation 5: Control of the Circulation

Question 1

What are the two main factors of autonomic regulation?

Answer 1

• vascular tone

- autonomic receptors (adrenergic and cholinergic)

Question 2

Describe the following components of vascular tone:

• basal tone
• resting sympathetic tone
• active mechanisms
• passive mechanisms

Answer 2

Basal Tone: Theoretical reference point. Amount of vascular contraction found under resting conditions without neural or hormonal (extrinsic) influences. (showing that without any input do have some tone between vascular smooth muscle cells, interaction between actin and myosin)

Resting Sympathetic Tone: Amount of vascular constriction found under resting conditions as a result of tonic sympathetic nerve activity. The resistance is higher than the basal arterial tone due to the presence of tonically-released norepinephrine.

Active mechanisms induce a change in vascular resistance away from the basal arterial tone.

Passive mechanisms induce a change in vascular resistance back toward the basal arterial tone.

Question 3

In resting conditions sympathetic tone will be at, above, or below basal tone? Why?

Answer 3

due to small increase in symp. nerve activity. when awake have background symp. nerve activity. when sleeping you withdraw symp. and are more parasympathetic.

Question 4

How is resistance affected if you increase sympathetic nerve activity?

Answer 4

resistance goes up bc of vessel vasoconstriction

Question 5

What is active vasoconstriction? What is the mechanism? Where is it in relation to the basal tone?

What happens if you withdraw sympathetic activation?

Answer 5

from basal tone get active vasoconstriction (norepi released on vascular smooth muscle cells, get more Ca coming in, and get more actin/myosin interaction) active vasoconstriction, more symp. tone, more constrict, if withdraw symp. activity get passive vasodilation- one of main ways ways in which symp. NS regulates vascular tone - activate alpha receptors, which causes vasoconstriction or withdraw symp. activity which causes passive vasodilation.

Question 6

What are sympathetic cholinergic fibers? What effect will they have?

Answer 6

symp. fibers that release Ach.
only in 3 tissues.

some in vascular system of skel. muscle which can cause vasodilation. releasing cholinergic get active vasodilation… if remove this symp. cholinergic then passive vasoconstriction) minor component but real. also work on pilorector muscles-hair stand up on neck.. symp. activity through cholinergics. mechanism when shivering -pilorector muscles, insulates skin if had lots of hair..) by far more important one is sympathetic aderergics which cause active vasoconstriction and passive vasodilation.

Question 7

How are adrenergic receptors stimulated? (chemically) Describe the receptors.

Answer 7

stimulated by isoproterenol, norepinephrine, epinephrine.

alpha (α) receptors - located on vascular smooth muscle; causes vasoconstriction. Coronary and cerebral vessels have little sympathetic vasoconstrictor innervation.

beta (β)-1 receptors - primary adrenergic receptor on cardiac muscle; stimulates heart rate and contractility.

beta (β)-2 receptors - secondary adrenergic receptor on cardiac muscle; stimulates heart rate and contractility.

beta (β)-2 receptors - primarily located on vascular smooth muscle; causes vasodilation.

Question 8

When do you give an alpha antagonist? When do you give an alpha agonist?

Answer 8

alpha antagonists- for hypertension to reduce vasoconstriction and reduce bp… shock give alpha agonist to try to vasoconstrict system to raise bp.

Question 9

When might you give a beta 1 blocker?

Answer 9

beta 1- on heart. stimulate increase in HR and contractility by stimulating Ca current, phospholamin, phos. of troponin I…

give beta 1 blocker to increase O consumption -reduces HR and contractility, don’t really stimulate beta 1 unless emergency situation

Question 10

What is the purpose of beta 2 receptors? What do they cause? Where are they located?/Why is this significant?

Answer 10

beta (β)-2 receptors - secondary adrenergic receptor on cardiac muscle; stimulates heart rate and contractility.

beta 2- seem to be similar in mech. to beta 1 but are diff. do cause background vasodilation. there are specific blockers for beta 1, beta 2. also located on vascular smooth muscle of bronchial dilators (relax vascular smooth muscle.allow you to bring in more air)…

Question 11

Do cholinergic receptors act on muscarinic or nicotinic receptors? What do they release? How are they blocked?

What type of receptor are endothelial cells?

Answer 11

Cholinergic Receptors - muscarinic receptors stimulated by acetylcholine (ACh). Blocked by atropine

(dont confuse w Ach released from neural tissue that innervates skel. muscle (those are neuromuscular junctions where Ach works on nicotinic receptor)

heart is only muscarininc. endothelial cells are muscarinic receptors.

Question 12

Describe both parasympathetic and sympathetic cholinergic receptors.

What do they innervate/act on?

Answer 12

parasympathetic fibers innervate a limited number of blood vessels; cerebral, some viscera including splanchnic, genitalia, bladder and large bowel; causes vasodilation. Skeletal muscle and cutaneous vessels are not innervated by parasympathetic nerves.

sympathetic cholinergic pathway - postganglionic sympathetic fibers that release acetylcholine on effectors. Ex. Sweat glands of nonapical skin to indirectly induce vasodilation.
(active vasodilators. located in sweat glands too to induce vasodilation. increases sweating. )

Question 13

Describe the baroreceptor reflex.

Answer 13

A negative feedback loop to control arterial pressure.

Arterial baroreceptors play a key role in short-term adjustments of blood pressure in response to relatively abrupt changes in blood volume (hemorrhage), cardiac output, or peripheral resistance.

Question 14

Where are baroreceptor nerve terminals located?

What is their function?

Where do afferent fibers join/go?

Answer 14

Baroreceptor nerve terminals are located in the walls of the carotid sinus (thin wall, allow better stretching) and aortic arch. These structures have relatively less vascular smooth muscle.

Baroreceptor nerve terminals respond to vascular stretch (mechanoreceptors) induced by changes in blood pressure.

Afferent nerve fibers from the carotid sinus and aortic arch join the ninth (glossopharyngeal) and tenth (vagus) nerves, respectively, to vasomotor centers in the medulla.

Question 15

When is baroreceptor nerve firing frequency increased or decreased?

Answer 15

Baroreceptor nerve firing frequency is increased by an increase in arterial pressure and decreased by a decrease in arterial pressure.

Question 16

Which is more sensitive to changes in bp; aortic arch or carotid sinus?

Answer 16

The carotid sinus baroreceptors are more sensitive than the aortic arch to changes in blood pressure.

Question 17

In regards to arterial pressure, what will stimulate sympathetic nerve activity? What results (through what mechanisms?)

Answer 17

A decrease in arterial pressure stimulates sympathetic and inhibits parasympathetic nerve activity leading to an increase in arterial pressure through:

1) peripheral vasoconstriction (+ sympathetic)
2) increase in heart rate (+ sympathetic and - parasympathetic)
3) increase in ventricular contractility (+ sympathetic)

(An increase in arterial pressure elicits the opposite neural responses, leading to a decrease in arterial pressure.)

Question 18

If you’re lying down then get up why don’t you always get dizzy?

Answer 18

don’t get dizzy bc baroreceptors monitoring bp constantly, as soon as you start to get up sympathetics increase your HR, and contractility, increase bp, and maintain constant bp in brain. also cerebral regulation- highly auto-regulated, maintains pressure on own, baroreceptors are additional mech..

Question 19

Where is the carotid sinus located? Describe it mechanically.

Answer 19

carotid sinus- thin wall, outpocking. allows better stretching of nerve fibers bc thin wall structure. located at internal carotid at bifurcation of internal/external carotid.

Question 20

Draw the baroreceptor feedback loop.

How might MAP affect the loop?

Answer 20

Slide 7.

looking at increase in MAP, really baroreceptors evolve more for hemorrhage (decrease in bp) or dehydration. hemorrhage more acute, dehydration more chronic. … increase in bp, stimulate baroreceptors, stretch, afferent pathway to brainstem, decrease symp. to blood vessels and decreases act. to heart -sinus node, lowers bp. … bradycardia and vasodilation counteract increase MAP.

decrease in MAP, reduce stretch on baroreceptor, reduce activity to brain, stimulate symp. to heart, stimulate symp. raise arterial bp.

Question 21

Are baroreceptors more responsive to pulsatile (phasic) pressures or constant (static) pressures?

Is absolute or

Answer 21

more responsive to phasic/pulsatile pressures.

baroreceptors more responsive to pulsatile phasic but responds to both

when mean bp high its more sensitive more stretched (doesn’t respond as well when low) can see that most firing, every time bp changes, what happens…during ejection of blood in aorta get big increase in firing, as declines get decrease in firing …not really responding to absolute pressure, responding to changes. Pressure same value at diff points… firing of baroreceptors respond to increase in pressure but not decrease in pressure quite same. rapid change causes rapid response. slow change, weak response. more impulses occur early than late.
has to do w rate of change… more important than absolute pressure.

Question 22

What is the blood pressure threshold for activation of sinus node impulses?

At a normal mean arterial pressure of 100 mmHg, when will carotid sinus nerve impulses be activated? How? Compare activation in early systole to late systole … why the difference?

How do receptors respond during diastole when pressure is still above threshold?

Answer 22

The blood pressure threshold for activation of sinus nerve impulses is about 50 mm Hg.

At normal mean arterial pressure (100 mm Hg) carotid sinus nerve impulses are activated in early systole by the increase (phasic change) in pressure.  Fewer impulses occur during late systole when pressure is still high but changing less. 

Note that when the pressure falls during diastole, the receptors reduce their firing rate even though the pressure is still above the threshold.

Graph slide 8.

Question 23

When the pulse pressure (phasic) is damped out but the mean arterial pressure is kept constant (static), what happens to the rate of neural activity from carotid sinus? How will systemic arterial pressure change and why?

Answer 23

the rate of neural activity recorded from the carotid sinus nerve decreases and systemic arterial pressure increases (due to less inhibition of sympathetic nerve activity and vasoconstriction). Restoring the pulse pressure in the carotid sinus restores the frequency of sinus nerve discharge and the systemic arterial pressure to control.

responding to phasic change and responds much less to constant pressure. restore pulsatile activity and carotid sinus responds more quickly.
responds to changes more than to absolute pressures- thats the point.

Question 24

How does hypertension affect baroreceptor sensitivity?

Draw graph (x axis arterial bp, y- baroreceptor discharge frequency).

Answer 24

Baroreceptor sensitivity decreases in hypertension.

In hypertension, a given increase in carotid sinus pressure elicits a lower frequency nerve response and therefore a smaller decrease in systemic arterial pressure than it does at normal blood pressure.

The threshold is increased and the receptors are less sensitive to changes in transmural pressure.

hypertension- baroreceptors dont fire more in person w hypertension bc don’t respond to steady changes as well. but shifts curve to right. same relationship but now at higher pressures. so baroreceptors adapt to hypertension. sensitivity decreases in hypertension- get to higher pressure to get response… but these people at higher pressure to begin with. (read #2)… people w hypertension don’t have much of a diff. threshold increased and baroreceptors less sensitive to higher pressure, but still respond to static changes that occur at higher pressure. so get to change in baroreceptors get to higher pressure.. but already at higher pressures

ppl w hypertension aren’t coming out w higher neural activity out of baroreceptors… sensitivity reduced. -thats point.

Graph slide 10.

Question 25

Where are peripheral chemoreceptors?

Where does the afferent nerve activity go?

Answer 25

Small highly vascular bodies located in the region of the aortic arch and just medial to the carotid sinus at the bifurcation of the internal and external carotid arteries (near the baroreceptors).

Afferent nerve activity from the carotid and aortic bodies is carried through the IX and X nerve, respectively, to the medulla (similar to the baroreceptors).

Question 26

How are peripheral chemoreceptors activated?

Answer 26

Primarily activated by low arterial PO2 but also is affected by high arterial PCO2 and low arterial pH (high H+).

peripheral chemoreceptors only play role during severe hypoxia. low O content. not activated during normal fluctuations of PaO2 levels.

Question 27

What do chemoreceptor signals stimulate? What is the actual effect? Why?

Answer 27

These signals stimulate efferent sympathetic and parasympathetic nerve activity to cause vasoconstriction and bradycardia, respectively.

In real life, however, hypoxia induces tachycardia because the increase in ventilation acts via stretch receptors in the lung to centrally inhibit efferent vagal nerve activity (resulting in an increase heart rate).
(bc increase in stretch receptors in ventilation in lungs.. take deep breath, inhibition of vagal activity, so sinus rate goes up when you inspire, and goes down when expire) same stretch receptors. inhibit vagal activity. increase in HR. effect of chemoreceptors alone- would cause vasoconstriction on bradycardia . but bc of lungs interfering wind up w tachycardia.

See diagram slide 12.

Hyperventilation causes alkalosis
Hypoventilation causes acidosis

Response to acidosis, from ischemia, body wants to blow off CO2, affect respiratory centers
VASOCONTRICTION occurs through stimulation of sympathetics, causing tachycardia
the respiratory effect excites PARASYMP activity causing BRADYCARDIA normally

Question 28

What tissue in body has highest blood flow per gram of tissue?

Answer 28

carotid body. v vascularized. designed to send O in blood

Question 29

Draw a graph that illustrates how percent maximum response changes with O2 concentration. How does high CO2 affect the graph?

How are chemoreceptors involved in both respiratory and CV system?

Answer 29

Slide 13.

go R to L as O content drops, percent maximum response of peripheral chemoreceptors. normal concentration of CO2 in blood around 40…look at middle line as normal. as O content falls, these fire more, but need low levels to get significant increase to affect heart. normal O content 100. when dropping arterial O content below 100 starts firing but really fires at low O content. as CO2 content goes up (goes along w decrease in O content) it shifts curve up and to R and makes more sensitive and they fire even more for any O. CO2 low then less sensitive, and need really low O to fire. so CO2 makes them more sensitive to drop in O. normal PaO2 around 100. normal PaCO2 around 40. middle line. more imp. in respiratory physiology.

(Chemoreceptors -Primarily involved with the regulation of respiration. Low O2 stimulates respiration.
Effects on the cardiovascular system are smaller than on the respiration system.)

Not as sensitive
Carotid body highest blood flow per gram of tissue sense O2 in the blood
Pa Co2 normal is 40, 100 Pa O2
CO2 makes them more sensitive to a drop in oxygen,
(High CO2 -Enhances response)

Question 30

Describe the hormonal control of the circulatory system. What is its mechanism responsible for? Draw flow chart.

Answer 30

Slide 14.

Renin-Angiotensin-Aldosterone

Primary mechanism responsible for long-term regulation of blood pressure.

involved in long term regulation of bp. involved to mitigate dehydration. this maintains arterial bp. not designed to mitigate hemorrhage (acute effect of low bp) doesn’t come into play w hemorrhage bc you wont last long enough. this mech. takes days if not longer. here’s low arterial bp… result of loss of fluid. hypovolemia. also kicks in (long term decrease in arterial bp

Question 31

What mechanism comes into play during hypoxia? What results? Why?

Answer 31

sensitive to decrease in PaO2. can be in conjunction w increase in CO2. respond to acidosis (generally occurs when O content drops, become ischemic, produce H ions) so peripheral chemoreceptors are activated and respiratory centers in brain. increase depth and rate of breathing. blow off CO2, increase O. CO2 is acid, hyperventilate reduce acidity in blood. when cant breathe you accumulate CO2 and turns into acid (acid carbonase. mechanism) chemoreceptors affect respiratory centers. in cardio-does affect CV center

effects will inhibit para. nerve activity. the efferent symp. and para. activity causes vasoconstriction and bradycardia dir. through CV center. but bc of effect on ventilation center, causes tachycardia (wind up w increase in HR) bc inhibits parasymp. so main effect is increase symp. nerve activity, causes widespread vasoconstriction of organs and venoconstriction and that raises your bp. vasoconstriction that raises diastolic bp. directly stimulates HR. idea bring more O and blood to organs. effect on parasym- direct stimulation will cause bradycardia but bc of ventilation system this inhibits para. (that overcomes the CV direct stimulation) system and causes increase in HR.
main mech. stimulate para.(get bradycardia) and sym. (get vasoconstriction) inhibit of HR… but HR winds up going up bc of respiratory input. stretch effects on lung- inhibits vagal activity, stimulate HR.
when stimulate symp. and parasym. at same time…para. usually win out but here doesn’t bc of respiratory effect inhibiting para.
designed to bring more O to tissues.

Question 32

How is the renin-angiotensin system involved in congestive heart failure?

What results? How do you treat?

Answer 32

congestive heart failure- sense decrease in arterial bp-kidneys sense that as hemorrhage.. so afferent renals- spec. cells… these arteriole vascular smooth muscle cells release renin. renin convert angiotensin- to angiotensin 1- precursor to angiotensin 2. on lungs and kidneys. enzymes that are Ace. angiotensin converting enzymes… they block conversion of angiotensin 1 to 2. normally 1 to 2 passes through lungs to kidneys bc those endothelial cells have Ace. ang.2 is most powerful vasoconstrictor in body… also stimulates release of aldosterone from adrenals -stimulates distal tubule in kidneys to reabsorb Na. … increase volume (follow chart). designed to mitigate dehydration

get increase in bp and increase in water reabsorption to bring volume back up. imp. in normal for dehydration but also mechanism invoked in congestive heart failure to increase fluid volume- NOT what you want. so give anti-diarhetics and one of them is a Ace inhibitor to prevent effects of antiotension to prevent raise of bp and reabsorption of fluid

Ace inhibitor- reduce volume and increase compliance of arterial system, lower bp.

Question 33

What is ADH?

Answer 33

ADH is anti diah. hormone-increase perm of collecting ducts of kidneys to reabsorb more water. bring more water into system.

Question 34

What is the first line of defense with congestive heart failure?

Answer 34

first line of defense in hypertension, if have hypertension want to get blood volume down, why? bc reduces compliance of vascular system. making pressures higher