Local Regulation of Blood Flow Flashcards

1
Q

How do changes in metabolic demand affect local blood flow?

A

Vasodilator intermediates produced by local tissues reduce arteriole smooth muscle tone and induce vasodilation to metabolically active tissue. (called active hyperemia)

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2
Q

What metabolites promote vasodilation?

A

Potassium, adenosine, nitric oxide, prostaglandins, hydrogen peroxide

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3
Q

How can a tissue overcome arteriole occlusion?

A

Vasodilating metabolites can increase locally and force the arteriole to open enough to allow an occlusion to pass (reactive hyperemia)

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4
Q

What is autoregulation?

A

A tissue can increase peripheral resistance in response to an increase in blood pressure (or vice versa) so that there is no change to local blood flow

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5
Q

In what two types of tissue is autoregulation especially strong?

A

Coronary and cerebral

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6
Q

What are the metabolic mechanisms of autoregulation?

A

If arterial pressure increases, local blood flow will increase. This causes local vasodilating metabolites to be washed away. The decrease then permits an increase in smooth muscle tone and vasoconstriction results

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7
Q

What is the myogenic mechanism of autoregulation?

A

Increase in arterial pressure will cause an increase in the stretching of local smooth muscle. This opens mechanical calcium channels which trigger contractions that induce vasoconstriction

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8
Q

From what compound is nitric oxide produced?

A

L-arginine

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9
Q

What are two means of triggering an increase in nitric oxide production?

A

Chemical (serotonin, Ach) or mechanical (blood flow shear forces)

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10
Q

What are two functions of nitric oxide?

A

1) Serves as a tonic vasodilator which modulates resistance on a local level
2) Inhibits platelet activity

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11
Q

What are two main local vasodilators?

A

Nitric oxide and prostacyclin

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12
Q

What are three main local vasoconstrictors (and two platlet activators)?

A

Endothelin (no platelet activity though)
Serotonin
Thromboxane

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13
Q

What are the two main neurotransmitters that the sympathetic nervous system uses in its postganglonic fibers?

A

Norepinephrine

Neuropeptide Y

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14
Q

What is the receptor target of sympathetic system in the heart? in the vasculature?

A

1) beta-adrenergic receptors

2) alpha receptors

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15
Q

How is the magnitude and duration of sympathetic activation limited?

A

Postganglionic nerve fibers have a norepinephrine reuptake mechanism in their nerve terminals; norepinephrine’s presence will inhibit further release. The presence of vasodilator metabolites will also prevent release

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16
Q

What are the main effects of sympathetic innervation in the arterioles and venules?

A

In arterial system: promotes vasoconstriction (increases resistance)
in venous system: reduces compliance

17
Q

In which tissues is sympathetic vasoconstrictive tone active?

A

Skin, inactive skeletal muscles, viscera, kidneys

18
Q

In which tissues is sympathetic vasoconstrictive tone inactivated?

A

Brain, heart, and active skeletal muscle

19
Q

What are the effects of the parasympathetic nervous system on blood flow?

A

Essentially none in the vasculature itself;

In the heart, lowers heart rate, atrial contractility, and A-V conduction

20
Q

What is the effect of hormonal norepinephrine on blood flow?

A
increases heart rate and contractility (beta-adrenergic)
increases vasoconstriction (alpha receptor)
21
Q

What is the effect of hormonal epinephrine on blood flow?

A

increases heart rate and contractility (beta-adrenergic)
increases vasoconstriction (alpha receptor–high concentrations)
increases vasodilation in skeletal muscle (beta receptor)

22
Q

What is the effect of hormonal renin on blood flow?

A

Responds to decreased arterial pressure to promote conversion of angiotensinogen to angiotensin I (which in turn becomes angiotensin II); angiotensin II promotes vasoconstriction

23
Q

What is the effect of hormonal vasopressin on blood flow?

A

Released from the posterior pituitary in response to low pressure; promotes vasoconstriction and in the kidneys promotes sodium and water reabsorption (ADH)

24
Q

What is the upstream pressure for blood delivery to the heart?

A

Since most coronary vessels are closed during ventricular contraction, aortic diastolic pressure is the driving force for blood flow

25
Q

How is coronary oxygen consumption calculated?

A

Coronary O2 consumption = Coronary blood flow * (PO2 of coronary arteries-PO2 of coronary veins)

26
Q

How is coronary work calculated?

A

Systolic arterial pressure x Heart Rate

27
Q

How are mismatches between oxygen delivered and oxygen required resolved?

A

Since the heart extracts most of the oxygen delivered to it, it must increase flow to gain more O2; thus it will increase vasodilating metabolites to promote more flow into the coronary vasculature

28
Q

How does ‘coronary steal’ work?

A

If a coronary vessel is partially occluded, it will not respond normally to local metabolite production, whereas normal vessels will. Normal vessels then will receive additional blood whereas the occluded vessels will actually lose blood due to their higher resistance

29
Q

What are the main local blood flow regulators for the brain?

A

Potassium, H+, NO, Adenosine, low O2

CO2 is an especially strong signal

30
Q

What type of control mechanisms predominate in exercising skeletal muscle?

A

Local (i.e. metabolic vasodilators)

31
Q

How does the body compensate for the increased demand to skeletal muscle that is working?

A

Sympathetics will
1) vasoconstrict inactive muscles and viscera
2) decrease venous compliance and force blood into heart [increase cardiac output]
3) increase heart rate and contractility
4) decrease parasympathetic involvement to heart
Active skeletal muscle also helps pump venous reservoir to heart

32
Q

What is the main role of vascular control in the skin?

A

Skin has low nutrient needs, so its vascular control is for body temperature control; vasoconstriction promotes retaining heat, vasodilation promotes heat dissipation