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LIU Chuan Yong

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Title: LIU Chuan Yong


1
LIU Chuan Yong ??? Institute of
Physiology Medical School of SDU Tel 88381175
(lab) 88382098 (office) Email
liucy_at_sdu.edu.cn Website www.physiology.sdu.edu.c
n
2
Section 4
  • Regulation of the Circulation

3
Introduction
  • The aim of the circulatory regulation is to
    regulate the blood flow of organs to fit their
    metabolic requirement in different condition.
  • The regulation of blood flow are of three major
    types
  • Neural
  • Humoral
  • Local

4
Neural control of blood flow
  • affects blood flow in large segments of the
    systemic circulation,
  • shifting blood flow from the non-muscular
    vascular bed to the muscles during exercise
  • changing the blood flow in the skin to control
    body temperature.

5
Humoral control
  • hormones, ions, or other chemicals in blood
  • cause either local increase or decrease in tissue
    flow
  • or widespread generalized changes in flow.

6
Local control of blood flow
  • in each individual tissue,
  • the flow being controlled mainly in proportion to
    that tissues need for blood perfusion

7
I. Neural Regulation of the Circulation
8
1. Innervation of the Circulatory System
  • Cardiac innervation
  • Innervation of blood vessels
  • Sympathetic vasoconstrictor fiber
  • Sympathetic vasodilator fiber
  • Parasympathetic nerve fiber to peripheral vessels

9
Cardiac innervation
  • Sympathetic nerve noradrenergic fiber
    Parasympathetic nerve- cholinergic fiber
  • Noradrenergic sympathetic nerve
  • to the heart increase the cardiac rate
    (chronotropic effect)
  • the force of cardiac contraction (inotropic
    effect).
  • Cholinergic vagal cardiac fibers decrease the
    heart rate.

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Cardiac innervation (contin.)
  • moderate amount of tonic discharge in the cardiac
    sympathetic nerves at rest
  • a good deal of tonic vagal discharge (vagal tone)
    in humans
  • When the vagi are cut in experiment animals, the
    heart rate rises

12
Innervation of blood vessels
  • Sympathetic vasoconstrictor fiber
  • Distribution Almost all segments of the
    circulation.
  • The innervation is powerful in the kidneys, gut,
    spleen and skin,
  • is less potent in both skeletal and cardiac
    muscle and in the brain.

13
Innervation of blood vessels
  • Sympathetic vasoconstrictor fiber (contin.)
  • Almost all vessels, such as arteries, arterioles,
    venules and veins are innervated,
  • except the capillaries, precapillary sphincters
    and most of the metarterioles.
  • Tone Usually the sympathetic vasoconstrictor
    fibers keep tonic.

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17
Innervation of blood vessels
  • 2) Sympathetic vasodilator fiber
  • The sympathetic nerves to skeletal muscles carry
    sympathetic vasodilator fibers as well as
    constrictor fibers.
  • In animals, such as the cat, dog, these
    sympathetic vasodilator fibers release
    acetylcholine at their endings and cause
    vasodilation.
  • Importance increase the blood flow in skeletal
    muscle during exercise and stress.

18
Innervation of blood vessels
  • 3) Parasympathetic nerve fiber to peripheral
    vessels
  • Parasympathetic nerve fibers innervate vessels of
    the blood vessels in
  • Meninges (??, ??)
  • the salivary glands,
  • the liver
  • the viscera in pelvis
  • the external genitals.
  • Importance Regulate the blood flow of these
    organs in some special situations.

19
2 Cardiovascular Center
  • The control center of cardiovascular activities
    is the nucleus groups at different levels for
    controlling cardiovascular activities,
  • including
  • spinal cord,
  • brain stem,
  • hypothalamus,
  • limbic system,
  • cerebral cortex
  • cerebellum.

20
Cardiovascular Center
  • if the brain of an anesthetized animal is
    sectioned at the level of the lower pons, the
    blood pressure falls.
  • If the section is made at the level of the obex,
    the fall in blood pressure is more profound.

21
Cardiovascular centers of the brainstem
  • Medulla oblongata is essential to Cardiovascular
    centers.

22
Cardiovascular centers of the brainstem
  • vasoconstrictor-area
  • vasodilator area
  • cardioinhibitory area
  • relay station of afferent nerve

23
1.rostral ventrolateral medulla,
rVLM (Vasoconstrictor area) 2. Caudal
ventrolateral medulla, cVLM(Vasodilator area) 3.
NTS (nucleu of solitary tract relay station of
afferent nerve) 4. Cardioinhibitory area
24
  • 1). vasoconstrictor-area (rVLM)
    (neurotransmitter NE neurons)
  • (l) the cardiac sympathetic center
  • (2) the sympathetic vasoconstrictor center

25
  • 2).vasodilator area (cVLM) (NE neurons)
  • to inhibit action of Cl area ? vasodilation

26
3).cardioinhibitory area (dorsal vagal nucleus
and nucleus ambigulus) the cardial vagus
center 4).relay station of afferent nerve
NTS (nucleu of solitary tract) to accept and
integrate afferent impulses and then affect
other centers
27
3. Reflex Regulation of the Circulation
  • Baroreceptor reflexes
  • Reflex involving arterial chemoreceptors
  • CNS ischemic response

28
(1) Baroreceptor reflexes
  • 1) Physiological anatomy of the baroreceptors.

29
Carotid sinus
  • At the bifurcation of the common carotid arteries
  • the root of internal carotid artery shows a
    little bulge
  • has stretch receptors in the adventitia
  • are sensitive to arterial pressure fluctuations

30
Carotid sinus.(contin.)
  • Afferent nerves from these stretch receptors
    travel in the carotid sinus nerve
  • which is a branch of the glossopharyngeal nerve.
    (IXth cranial nerve)

31
Aortic arch.
  • baroreceptors are also present in the adventitia
    of the arch of aorta
  • have functional characteristics similar to the
    carotid sinus receptors.
  • their afferent nerve fibers travel in the aortic
    nerve,
  • which is a branch of the vagus nerve. (Xth
    cranial nerve)

32
2) buffer nerves activity
  • The carotid sinus nerves and vagal fibers from
    the aortic arch are commonly called the buffer
    nerves
  • At normal blood pressure levels, the fibers of
    the buffer nerve discharge at a low rate.
  • When the pressure in the sinus and aortic arch
    rises, the discharge rate increases
  • when the pressure falls, the rate declines.

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34
Sinus Nerve response to Blood Pressure
  • The carotid sinus baroreceptors are not
    stimulated by intrasinus pressure between 0 60
    mmHg (aortic baroreceptors, 0-30mmHg).
  • Between 60 to 80 mmHg, the carotid sinus
    baroreceptors respond progressively more and more
    strongly.
  • The response is the greatest at pressure level
    near the normal mean arterial pressure (100
    mmHg).
  • At sinus pressure above 180 mmHg, there is no
    further increase in response .

35
3) Relationship between the isolated carotid
sinus pressure and the blood pressure
  • Raising the carotid sinus pressure leads to a
    fall in arterial blood pressure.

36
  • Lowering the carotid sinus pressure leads to a
    rise in arterial blood pressure

CSP, carotid sinus pressure FABP, femoral artery
blood pressure
37
  • Set point The point where the carotic sinus
    (isolated) pressure and blood pressure are the
    same.

38
4) Concept and mechanism of baroreceptor reflex
  • Any drop in systemic arterial pressure decreases
    the discharge in the buffer nerves,
  • and there is a compensatory rise in blood
    pressure and cardiac output.
  • Any rise in blood pressure produce dilation of
    the arterioles and decreases cardiac output until
    the blood pressure returns to its previous normal
    level.

39
Carotid Sinus Aortic Arch
Sinus Nerve
Arterial Pressure
Baroreceptor
Vagus Nerve
Vasoconstrictor Center
Peripheral Vascular Dilation
Cardio-acceleratory Area
Heart Rate Contractility
Cardio-inhibitory Area
Peripheral Resistance ( R)
Arterial pressure decrease back towards normal
Cardiac Output (Q)
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43
(5) Importance of the baroreceptor reflex
  • To keep the arterial pressure relatively constant
  • Through short term regulation of blood pressure
    in the rang of 70 mmHg to 150 mmHg, maintain the
    mean blood pressure at about 100 mmHg
  • Tonic regulation of blood pressure
  • Pressure buffer system reduce the blood
    fluctuation during the daily events, such as
    changing of the posture, respiration, excitement,
    and so forth.

44
(6) Baroreceptor Resetting
  • Baroreceptor will adapt to the long term change
    of blood pressure.
  • That is, if the blood pressure is elevated for a
    long period of time, several days or years, the
    set point will transfer to the elevated mean
    blood pressure.
  • Obviously, the adaptation of the baroreceptor
    prevents the baroreceptor reflex from acting as a
    long term control system.
  • That makes the baroreceptor system unimportant
    for long-term regulation of arterial pressure

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46
(2) Reflex involving arterial chemoreceptors
  • Chemoreceptors situated in the carotid body and
    aortic body

47
  • They have a very rich blood supply,
  • which make them ideal for sampling chemical
    changes in the blood.
  • Chemoreceptors are sensitive to the decreased
    Po2, increased PCO2 and increased hydrogen ion
    concentration in the plasma.
  • Afferent
  • Afferent nerve fibers form the carotid body
    travel in the carotid sinus nerve, which is a
    branch of glossopharyngeal nerve.
  • Aortic body is innervated by the aortic nerve,
    which is a branch of the vagus

48
  • Response Stimulation of chemoreceptors leads to
    a reflex increase in vasomotor tone,
  • which causes generalized vasoconstriction and
    hence a rise in blood pressure.
  • Importance Chemoreceptor mechanism is important
    in regulation of blood pressure when it fall
    below the range in which baroreceptors act (70
    mmHg).

49
(3) CNS ischemic response
  • Chemoreceptor reflex is useful in regulation of
    blood pressure when it falls to a level between
    40 and 70 mmHg.
  • But if the blood pressure below 40 mmHg, the last
    ray of hope for survival is the central nervous
    system (CNS) ischemia response.
  • So it sometimes called the last ditch stand
    pressure control mechanism.

50
  • As the name indicates, it is evoked by ischemia
    (poor blood flow) of the central nervous system.
  • CNS ischemia reduces blood flow to the vasomotor
    centre (VMC).
  • Reduction in blood flow to the VMC leads to
    reduced Po2 and elevated Pco2 in the medulla
    region.
  • Both these factors stimulate the VMC directly,
    leading to vasoconstriction and consequently rise
    in blood pressure.

51
II Chemical and hormonal control of
cardiovascular function
52
Introduction
  • Various hormones, chemicals
  • Start at a low pace,
  • Have long-lasting influences on cardiovascular
    function.
  • Hormones and chemicals are classified into two
    groups
  • Vasoconstrictors
  • Vasodilators

53
Vasoconstrictors and Vasodilators
  • Vasoconstrictors
  • Epinephrine and Norepinephrine
  • Angiotensin II
  • Vasopressin
  • Vasodilators
  • EDRF (NO)

54
Epinephrine and Norepinephrine
  • The adrenal medulla secrete both epinephrine
    (80) and norepinephrine (20)
  • carried by blood flow to everywhere in the body.
  • In the blood, only a little norepinephrine comes
    form the endings of the adrenergic fibers.

55
Adrenergic receptors
a1 receptor on vessels ß1 receptor on heart ß2
receptor on vessels (skeletal muscle and liver)
Vasoconstriction Positive effect Vasodilation
Epinephrine Norepinephrine
56
Effect
  • On heart in vitro (contractility and
    automaticity).
  • both increase the force and rate of contraction
    of the isolated heart.
  • mediated by ß1 receptors.

57
Effect
  • On peripheral resistance.
  • Norepinephrine produces vasoconstriction in most
    if not all organs via a1 receptors
  • epinephrine dilates the blood vessels in skeletal
    muscle and the liver via ß2 receptors.
  • overbalances the vasoconstriction produced by
    epinephrine elsewhere, and the total peripheral
    resistance drops.

58
Effect
  • On heart in vivo (heart rate and cardiac output).
  • When norepinephrine is infused introvenously
  • the systolic and diastolic blood pressure rise.
  • The hypertension stimulates the carotid and
    aortic baroreceptors,
  • producing reflex bradycardia that override the
    direct cardioacceleratory effect of
    norepinephrine.
  • Consequently, the heart rate and cardiac out
    falls.

59
Effect
  • On heart in vivo
  • Epinephrine causes a widening of the pulse
    pressure
  • baroreceptor stimulation is insufficient to
    obscure the direct effect of the hormone on the
    heart,
  • cardiac rate and output increase.

60
Angiotensin II
  • very potent vasoconstrictor
  • formed in the plasma through a chain reaction.
  • The chain is triggered by a substance, renin,
    released form kidneys.
  • Renin is released from kidneys in response to
    renal ischemia, which may be due to a fall in
    blood pressure.

61
Effect of Angiotensin II
  • powerful constrictor
  • release aldosterone from the adrenal cortex
  • acts on the brain to create the sensation of
    thirst.
  • inhibit the baroreceotor reflex and
  • increase the release of norepinephrine from the
    sympathetic postganglionic fiber.

62
Vasopressin
  • Also called antidiuretic hormone (ADH),
  • formed in the hypothalamus (mainly)
  • secreted through the posterior pituitary gland.
  • even more powerful than angiotensin as a
    vasoconstrictor.
  • The high concentration of vasopressin during
    hemorrhage can raise the arterial pressure as
    much as 40 to 60 mmHg.

63
Vasopressin
  • The amount of endogenous vasopressin in the
    circulation of normal individuals does not
    normally affect blood pressure.
  • it does not increase blood pressure when small
    doses are injected in vivo
  • Acts on the brain to cause a decrease in cardiac
    output.
  • (in the area of postrema, one of the
    circumventricular organs)
  • Acts on the kidney

64
Endothelium Derived Relaxing Factor
  • Metabolism

65
Effect of NO
  • Relax the vascular smooth muscle directly
  • Mediate vascular dilator effect of some hormones
    and transmitters (Ach, bradykinin, VIP, substance
    P)
  • Inhibit the tonic excitation of some neurons in
    the vasomotor centre.
  • Inhibit the norepinephrine release from the
    sympathetic postganglionic fiber.
  • One or more of these effects are physiological.

66
III Autoregulation of Local Blood Pressure
  • Role of Vasodilator Substances.
  • CO2, Lactic acid, Adnosine, Adnosine phosphate
    compounds, Histamine, K and H
  • Myogenic Activity
  • Heterometric autoregulation

67
IV Long-Term mechanism for Arterial Pressure
Regulation
  • Renal body Fluid Mechanism

68
V Summary of the Integrated Multifaceted System
for Arterial Pressure Regulation
69
Introduction
  • Arterial pressure is regulated but by several
    interrelated systems
  • each of which performs a specific function.

70
If the blood pressure drops suddenly
  • two problems confronts the pressure control
    system
  • The first is survival,
  • to return the arterial pressure immediately to a
    high enough level
  • that the person can live trough the acute
    episode.

71
If the blood pressure drops suddenly
  • The second is to return the blood volume
    eventually to its normal level
  • so that the circulatory system can re-establish
    full normality,
  • including return of the arterial pressure all the
    way back to its normal value

72
Three kind of mechanisms in regulating the blood
pressure
  • react rapidly, within seconds or minutes
  • respond over an intermediate time period, minutes
    or hours
  • provide long-term pressure regulation, days,
    months, and years.

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1, Rapidly Acting Pressure Control Mechanisms,
Acting Within Seconds or Minutes
  • The baroreceptor feedback mechanism.
  • The central nervous system ischemic mechanism.
  • The chemoreceptor mechanism

75
Effect of Rapidly Acting Pressure Control
Mechanisms
  • To cause constriction of the veins and provide
    transfer of blood into the heart.
  • To cause increased heart rate and contractility
    of the heart and provide greater pumping capacity
    by the heart
  • To cause constriction of the peripheral
    arterioles to impede the flow of the blood out of
    the arteries.
  • All these effects occur almost instantly to raise
    the arterial pressure back into a survival range.

76
2. Pressure Control Mechanisms That Act After
Many Minutes
  • The renin-angiotensin vasoconstrictor mechanism
  • Stress-relaxation of the vasculature
  • Shift of fluid through the tissue capillary wall
    in and out of the circulation to adjust the blood
    volume as needed.

77
(1) The renin-angiotensin vasoconstrictor
mechanism
78
(2) Stress-relaxation of the vasculature
  • When the pressure in the blood vessels becomes
    too high,
  • they become stretched and keep on stretching
    more and more for minutes or hours
  • as a result, the pressure in the vessels falls
    toward normal.
  • This continuing stretch of the vessels, called
    stress-relaxation, can serve as an
    intermediate-term pressure buffer.

79
(3) Shift of fluid through the tissue capillary
wall in and out of the circulation
  • any time the capillary pressure falls too low,
  • fluid is absorbed by capillary osmosis from the
    tissue into the circulation,
  • thus building up the blood volume and increasing
    the pressure in the circulation.

80
Pressure Control Mechanisms That Act After Many
Minutes
  • become mostly activated within 30 minutes to
    several hours.
  • can last for long periods, days if necessary.
  • During this time, the nervous mechanisms usually
    fatigue and become less and less effective

81
3, Long-Term Mechanisms for Arterial Pressure
Regulation
  • The renal blood volume pressure control
    mechanism.
  • Aldosterone
  • Importance
  • It takes a few hours to show significant response
    for these mechanisms.
  • Return the arterial pressure all the way back.

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