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Physiology > Lecture 12: Control Of Blood Flow > Flashcards

Lecture 12: Control Of Blood Flow Flashcards

1
Q

What are the two phases and characteristics of each for local blood flow control?

A
  • Acute control:
  • Rapid changes in local vasodilation/vasoconstriction
  • Occurs in seconds to minutes
  • Basic theories:
    • Vasodilator theory
    • Oxygen (nutrient) lack theory
  • Long-term control:
  • Increase in sizes/numbers of vessels
  • Occurs over a period of days, weeks, or months
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2
Q

Describe the vasodilator theory

A
  • As metabolism increases, oxygen levels decrease.
  • This initiates the formation of Vasodilators
  • Examples: Adenosine Carbon dioxide Adenosine phosphate compounds Histamine Potassium ions Hydrogen ions
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3
Q

Describe the oxygen (nutrient) Lack Theory:

A

As Oxygen levels go down, the blood vessels must relax through Vasodilation

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4
Q

Define Vasomotion

A

Def: Cyclical opening and closing of precapillary sphincters.

  • Number of precapillary sphincters open at any given time is roughly proportional to nutritional requirements of tissues. The assumption is that smooth muscles require oxygen to remain contracted.
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5
Q

Describe Hyperemia

A

Can be either reactive or active.

  • Reactive:
    • Tissue blood flow is blocked; can be for seconds, hours, or more.
    • When unblocked, blood flow increases up to 4-7x normal. This is Reactive Hyperemia
  • Active:
    • When any tissue becomes active, rate of blood flow 8 Active: increases.
  • See Slides 9-11
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6
Q

Describe autoregulation.

What are two views that potentially explain autoregulation

A

In any tissue:

  • Rapid increase in arterial pressure leads to increased blood flow.
  • Within minutes, blood flow returns to normal even with elevated pressure.

Views to explain autoregulation:

  • Metabolic theory
  • Myogenic theory
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7
Q

What are the basic differences between metabolic and myogenic theory?

A

Metabolic:
Increase in Blood Flow -> Too Many Nutrients or Too Much Oxygen -> Washes out Vasodilators, allowing reconstriction

Myogenic:
Stretching of Vessels -> Reactive Vasoconstriction

We aren’t sure which theory is true.
- See Slide 14

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8
Q

Describe Blood Flow control Measures in the kidneys, brain, and skin

A
  • Kidneys:
  • Tubuloglomerular feedback:
    • Involves the macula densa/juxtaglomerular apparatus
  • Brain
  • Hydrogen and/or CO2 goes up -> Verebral Vessel Dilation -> Washing out of excess CO2/H+
  • Skin
    Blood flow linked to body temperature
  • Sympathetic nerves via CNS
  • 3 ml/min/100 g tissue →7-8 L/min for entire body
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9
Q

Describe Endothelial-Derived Mechanisms (For Control of Tissue Blood Flow)

A
  • Healthy Endothelial Cells -> Nitric Oxide Release
  • Nitric Oxide allows cGTP to be converted to cGMP in vascular smooth muscle cells…
  • …which activates protein kinases that lead to Vasodilation

Hypertension occurs when:

  • Damaged Cells, such as those that prevent Nitric Oxide to work properly, lead to the production of a peptide called endothelin,
  • Which leads to vasoconstriction
  • May wanna read this chapter for reals.
  • And also, see slide 18
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10
Q

Describe Humoral Circulation Controls for Vasoconstriction

A
  • Norepinephrine
  • Epinephrine
  • Angiotensin II - Normally acts to increase total peripheral resistance
  • Vasopressin - aka = ADH; very powerful vasoconstrictor; major function is to control body fluid volume
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11
Q

Describe Humoral Circulation Control for Vasodilation

A
  • Bradykinins - Causes both vasodilation and increased capillary permeability.
  • Histamine - Powerful vasodilator derived from mast cells and basophils)
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12
Q

What is the purpose of the sympathetic system?

A
  • Innervates all vessels except capillaries
  • Primarily results in vasoconstriction
  • See Slides 22, 23
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13
Q

Where is the vasoconstrictor and the vasodilator area of the brain located

A
  • Vasoconstrictor area:
  • Anterolateral portions of upper medulla
  • Transmits continuous signals to blood vessels:
    • Continual firing results in sympathetic vasoconstrictor tone.
    • Partial state of contraction of blood vessels = vasomotor tone.
  • Vasodilator area:
  • Bilateral in the anterolateral portions of lower medulla
  • Inhibits activity in vasoconstrictor area
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14
Q

Where is the vasomotor sensory and the higher nervous control centers of the brain located?

A
  • Sensory area:
  • Bilateral in tractus solitarius in posterolateral portion of medulla
  • Receives signals via:
    • Vagusnerves (CN X)
    • Glossopharyngeal nerves (CN IX)
  • Controlled by higher nervous centers:
  • Reticular substance (RAS)
  • Hypothalamus
  • Cerebral cortex

See Slides 26, 27

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15
Q

What is the adrenal medulla

A

Secretes epinephrine and norepinephrine

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16
Q

What occurs during neural rapid control of arterial pressure?

A
  • Simultaneous changes:
    • Constriction of most systemic arteries
    • Constriction of veins
    • Increased heart rate
  • Rapid response (within seconds)
  • Increased blood pressure during exercise (accompanied by vasodilation)
  • Alarm reaction (fight or flight)
  • See Slide 30
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17
Q

Where are baroreceptors located

A
  • Located in carotid sinuses and aortic sinus:
  • Stimulated by low arterial pressures:
    • Carotid sinuses are stimulated by pressure > 60 mm Hg
    • Aortic sinus is stimulated by pressure > 30 mm Hg
    • Vagus nerves (CN X)
  • Glossopharyngeal nerves (CN IX) via small Herring’s nerves (carotid baroreceptors)
  • Reticular substance (RAS)
  • Hypothalamus
  • Cerebral cortex
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18
Q

Describe the signals from baroreceptors

A
  • Inhibit vasoconstrictor center
  • Excite vasodilator center
  • Signals cause either increase or decrease in arterial pressure.
  • Primary function is to reduce the minute-by-minute variation in arterial pressure.
  • See Slides 34-38
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19
Q

Describe Chemoreceptors

A
  • Located in carotid bodies in bifurcation of the common carotids and in aortic bodies.
  • Chemosensitive cells sensitive to lack of oxygen, carbon dioxide excess, and hydrogen ion excess.
  • Signals pass through Herring’s nerves and vagus nerves.
  • Play a more important role in respiratory control.
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20
Q

Describe atrial reflexes

A
  • Low pressure receptors are located in the atria and pulmonary arteries and play an important role in minimizing arterial pressure changes in response to changes in blood volume.
  • Increase in atrial stretch results in:
  • Reflex dilation of kidney afferent arterioles
  • Increases kidney fluid loss
  • Decreases blood volume
  • Increase in heart rate (via CN X to medulla)
  • Signals to hypothalamus to reduce [ADH]
  • Atrial natriuretic peptide (ANP) -> Kidneys
  • Peptide in Kidneys Increase GFR, and Decrease Sodium Reabsorption
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21
Q

Describe arterial pressure relationship with kidneys

A
  • Arterial pressure = cardiac output X total peripheral resistance
  • Arterial pressure rises when total peripheral resistance is acutely increased.
  • Normal functioning kidneys return the arterial pressure back to normal within a day or two:
    • Pressure diuresis
    • Pressure natriuresis
  • See Slide 42
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22
Q

What are the characteristics of primary hypertension

A
  • Increased cardiac output
  • Increased sympathetic nerve activity
  • Increase in angiotensin II and aldosterone levels
  • Impairment of renal-pressure natriuresis mechanism
  • Inadequate secretion of salt and water
  • Primary (essential hypertension):
  • Hypertension of unknown origin
  • 90 –95% of hypertension
  • Major factors include:
    • Weight gain, characterized by: Increased cardiac output, Increased sympathetic nerve activity, Increased antiotensin II and aldosterone levels, and Impaired renal-pressure natriuresis mechanism
  • -Sedentary life style
23
Q

Describe secondary hypertension

A
  • Hypertension second to some other cause:
  • Tumor affecting renin-secreting juxtaglomerular cells
  • Renal artery constriction
  • Coarctation of the aorta
  • Preeclampsia
  • Neurogenic hypertension
  • Genetic causes
24
Q

What are renal-based causes of hypertension?

A
  • Chronic renal disease
  • Renal artery stenosis
  • Renin-producing tumors
  • Acute glomerulonephritis
  • Polycystic disease
  • Renal vasculitis
25
Q

What are endocrine-based causes of hypertension?

A
  • Cushing syndrome (adrenocortical hyperfunction)
  • Exogenous hormones (i.e., glucocorticoids, estrogen)
  • Pheochromocytoma
  • Acromegaly
  • Hypothyroidism (myxedema)
  • Hyperthyroidism (thyrotoxicosis)
  • Pregnancy induced
26
Q

What are cardiovascular-based causes of hypertension

A
  • Coarctation of the aorta
  • Polyarteritis nodosa
  • Increased intravascular volume
  • Rigidity of the aorta
  • Increased cardiac output
27
Q

What are neurological-based causes of hypertension?

A
  • Psychogenic
  • Increased intracranial pressure
  • Sleep apnea
  • Acute stress
28
Q

What are contributing factors to hypertension

A
  • Genetic factors (Essential hypertension is a complex multifactorial disorder)
  • Other single-gene disorders that alter sodium reabsorption by the kidneys
  • Genetic variants in the renin-angiotensin system
  • Stress
  • Obesity
  • Smoking
  • Physical inactivity
  • Heavy consumption of salt
29
Q

What are Factors resulting in decreased peripheral resistance (vessel dilation) leading to decreased blood pressure

A
  • Increased production of nitric oxide
  • Increased release of prostacyclin
  • Increased release of kinins
  • Increase in atrionatriuretic peptide (ANP)
  • Decreased neural factors (β-adrenergic)
30
Q

What are Factors resulting in decreased cardiac output leading to decreased blood pressure

A
  • Decreased blood volume
  • Decreased heart rate
  • Decreased contractility
31
Q

What are hypertension factors resulting in increased cardiac output leading to increased blood pressure

A
  • Increased heart rate
  • Increased contraction
  • Increased blood volume (due to aldosterone)
32
Q

What are hypertension factors resulting in increased peripheral resistance leading to increased blood pressure

A
  • Increased angiotensin II
  • Increased catecholamines
  • Increased thromboxane
  • Increased neural factors (α-adrenergic)
33
Q

List examples of humoral vasoconstrictors and vasodilators.

A
  • Vasoconstrictors:
  • Angiotensin II
  • Catecholamines
  • Endothelin
  • Vasodilators:
  • Kinins
  • Prostaglandins
  • Nitric oxide
34
Q

What are the lethal effects of chronic hypertension?

A
  • Early heart failure and coronary artery disease
  • Cerebral infarct
  • Kidney failure
35
Q

What are characteristics of atherosclerosis

A
  • Atherosclerosis is a type of arteriosclerosis (“hardening of the arteries”).
  • The major characteristic of atherosclerosis is the presence of lesions within the intima of the vessel wall that protrude into the vessel lumen.
36
Q

What are non-modifiable (constitutional) risk factors of atherosclerosis?

A
  • Age:
  • Risk increases between the ages of 40 and 60.
  • Death rates from ischemic heart disease increase with each decade.
  • Gender:
  • Uncommon in premenopausal women without other risk factors
  • Increases after menopause and eventually exceeds that of men
  • Genetics:
  • Some Mendelian disorders associated with atherosclerosis but mostly multifactorial
37
Q

What are modifiable risk factors of atherosclerosis?

A
  • Hyperlipidemia (esp., hypercholesterolemia):
  • Major risk factor
  • Correlated with high levels of LDL (carries cholesterol to peripheral tissues) as opposed to HDL (carries cholesterol to liver)
  • Hypertension
  • Increases risk of IHD by 60%
  • Most important cause of left ventricular hypertrophy
  • Cigarette smoking
  • Diabetes
38
Q

What are other risk factors of atherosclerosis?

A
  • Inflammation
  • Hyperhomocystinemia
  • Metabolic Syndrome
  • Lipoprotein(a)
  • Factors affecting Hemostasis
  • Lifestyle (Including Lack of Exercise, Competitive/Stressful lifestyle, and Obesity)
39
Q

How does inflammation contribute as a risk factor to atherosclerosis?

A
  • Intimately linked with atherosclerotic plaque formation
  • C-reactive protein (CRP) is a major marker for inflammation.
  • Synthesized by liver
  • Plays important role in opsonizing bacteria and activating complement
  • Correlated with high levels of LDL (carries cholesterol to peripheral tissues) as opposed to HDL (carries cholesterol to liver)
40
Q

How does hyperhomocystinemia contribute as a risk factor to atherosclerosis?

A
  • Inborn error of metabolism

- Associated with premature vascular disease

41
Q

How does metabolic syndrome contribute as a risk factor to atherosclerosis?

A
  • Associated with insulin resistance:
  • Characteristics:
    • Obesity (esp. abdominal fat)
    • Insulin resistance
    • Fasting hyperglycemia
    • Increased lipid triglycerides
    • Decreased HDL levels
    • Hypertension
42
Q

What factors can cause endothelial injury or dysfunction?

A
  • Results in intimal thickening
  • May lead to formation of atheroma in presence of hyperlipidemia
  • Factors related to endothelial dysfunction:
    • Hypertension
    • Hyperlipidemia
    • Cigarette smoke
    • Homocysteine
    • Infectious agents
    • Hemodynamic disturbances
    • Hypercholesterolemia
43
Q

What can cause an accumulation of lipoproteins? (Especially LDL)

A
  • Result of chronic hyperlipidemia (esp. hypercholesterolemia)
  • Lipoproteins accumulate in the intima and are oxidized by oxygen free radicals generated by macrophages or endothelial cells.
  • Oxidized LDL is ingested by macrophages which become foam cells.
  • Oxidized LDL stimulates release of growth factors, cytokines, and chemokines.
  • Oxidized LDL is toxic to endothelial cells and smooth muscle cells.
44
Q

What factors are associated with monocyte adhesion to the endothelium?

A
  • Endothelial cells express VCAM-1 adhesion molecules that bind monocytes and T cells to endothelium.
  • Monocytes transform into macrophages and engulf lipoproteins.
  • T cells stimulate a chronic inflammatory response.
  • Activated leukocytes and endothelial cells release growth factors that promote smooth muscle cell proliferation
45
Q

How is smooth muscle proliferation linked as a risk factor to atherosclerosis?

A
  • Intimal smooth muscle cell proliferation and extracellular matrix deposition converts a fatty streak into a mature atheroma.
46
Q

What is the morphology of atheroma?

A

An atheroma consists of a cap of smooth muscle cells, macrophages, foam cells (converted macrophages), and other extracellular components, overlying a necrotic center composed of cell debris, cholesterol, foam cells, and calcium.

47
Q

What are the developmental stages of atherosclerosis?

A
  • Earliest lesions are fatty streaks:
    • Note these are also seen in all children older than 10.
  • Atherosclerotic plaques impinge on the lumen of the artery and grossly appear white or yellow.
  • Plaques progressively enlarge due to cell death and degeneration and synthesis/degradation of extracellular matrix.
  • Plaques often undergo calcification.
  • Plaques may rupture, ulcerate, or erode.
48
Q

What are the most common arterial sites for atherosclerosis?

A

Ranked from Most Involved to Least:

  • Lower abdominal aorta
  • Coronary arteries
  • Popliteal arteries
  • Internal carotid arteries
  • Circle of Willis
  • See Slide 68
49
Q

What are short-term and long-term controls of arterial pressure?

A
  • Short term control of arterial pressure:
  • Via sympathetic nervous system effects on:
    • Total peripheral vascular resistance and capacitance
    • Cardiac pumping ability
  • Long term control of arterial pressure:
  • Via multiple nervous and hormonal controls
  • Via local controls in kidney that regulate:
    • Salt and water excretion
  • See Slide 70, 71
50
Q

What is the relation of arterial pressure and kidney output?

A
  • As arterial pressure goes up, urine output goes up, causing pressure diuresis
  • As arterial pressure goes up, sodium output goes up, causing pressure natriuresis
  • Return of the arterial pressure always back to the equilibrium point = Near Infinite Feedback Gain Principle.
  • Primary determinants of the long-term arterial pressure level:
    • Degree of pressure shift of the renal output curve for water/salt
    • Level of water/salt intake
  • SEE SLIDES 73-76
51
Q

Define Chronic Hypertension

A

Definition:

  • One’s mean arterial pressure is greater than the upper range of the accepted normal measure.
  • Normal: 90 mm Hg (110/70)
  • Hypertensive: 110 mm Hg (135/90)
  • Severe hypertensive: 150/170 (250/130)
  • See Slide 79-80
52
Q

What are the lethal effects of chronic hypertension?

A
  • Early heart failure
  • Coronary heart disease
  • Heart attack
  • Cerebral infarct
  • Destruction of kidney areas->kidney failure->uremia->death
53
Q

See Slides 83-88

A

Consider making more flashcards on this part.

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