Lecture 12: Control Of Blood Flow Flashcards Preview

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Flashcards in Lecture 12: Control Of Blood Flow Deck (53):
1

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

* 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

2

Describe the vasodilator theory

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

3

Describe the oxygen (nutrient) Lack Theory:

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

4

Define Vasomotion

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.

5

Describe Hyperemia

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

6

Describe autoregulation.

What are two views that potentially explain autoregulation

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

7

What are the basic differences between metabolic and myogenic theory?

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

8

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

* 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

9

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

- 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

10

Describe Humoral Circulation Controls for Vasoconstriction

- 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

11

Describe Humoral Circulation Control for Vasodilation

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

12

What is the purpose of the sympathetic system?

- Innervates all vessels except capillaries
- Primarily results in vasoconstriction
- See Slides 22, 23

13

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

* 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

14

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

* 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

15

What is the adrenal medulla

Secretes epinephrine and norepinephrine

16

What occurs during neural rapid control of arterial pressure?

- 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

17

Where are baroreceptors located

* 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

18

Describe the signals from baroreceptors

- 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

19

Describe Chemoreceptors

- 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.

20

Describe atrial reflexes

- 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

21

Describe arterial pressure relationship with kidneys

* 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

22

What are the characteristics of primary hypertension

- 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

Describe secondary hypertension

* 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

What are renal-based causes of hypertension?

- Chronic renal disease
- Renal artery stenosis
- Renin-producing tumors
- Acute glomerulonephritis
- Polycystic disease
- Renal vasculitis

25

What are endocrine-based causes of hypertension?

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

26

What are cardiovascular-based causes of hypertension

- Coarctation of the aorta
- Polyarteritis nodosa
- Increased intravascular volume
- Rigidity of the aorta
- Increased cardiac output

27

What are neurological-based causes of hypertension?

- Psychogenic
- Increased intracranial pressure
- Sleep apnea
- Acute stress

28

What are contributing factors to hypertension

- 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

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

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

30

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

- Decreased blood volume
- Decreased heart rate
- Decreased contractility

31

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

- Increased heart rate
- Increased contraction
- Increased blood volume (due to aldosterone)

32

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

- Increased angiotensin II
- Increased catecholamines
- Increased thromboxane
- Increased neural factors (α-adrenergic)

33

List examples of humoral vasoconstrictors and vasodilators.

* Vasoconstrictors:
- Angiotensin II
- Catecholamines
- Endothelin
* Vasodilators:
- Kinins
- Prostaglandins
- Nitric oxide

34

What are the lethal effects of chronic hypertension?

- Early heart failure and coronary artery disease
- Cerebral infarct
- Kidney failure

35

What are characteristics of atherosclerosis

- 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

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

* 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

What are modifiable risk factors of atherosclerosis?

* 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

What are other risk factors of atherosclerosis?

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

39

How does inflammation contribute as a risk factor to atherosclerosis?

- 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

How does hyperhomocystinemia contribute as a risk factor to atherosclerosis?

- Inborn error of metabolism
- Associated with premature vascular disease

41

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

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

42

What factors can cause endothelial injury or dysfunction?

- 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

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

- 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

What factors are associated with monocyte adhesion to the endothelium?

- 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

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

- Intimal smooth muscle cell proliferation and extracellular matrix deposition converts a fatty streak into a mature atheroma.

46

What is the morphology of atheroma?

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

What are the developmental stages of atherosclerosis?

- 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

What are the most common arterial sites for atherosclerosis?

Ranked from Most Involved to Least:
- Lower abdominal aorta
- Coronary arteries
- Popliteal arteries
- Internal carotid arteries
- Circle of Willis

- See Slide 68

49

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

* 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

What is the relation of arterial pressure and kidney output?

- 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

Define Chronic Hypertension

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

What are the lethal effects of chronic hypertension?

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

53

See Slides 83-88

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