Lecture 11 Control of Blood Flow Flashcards
1
Q
Describe Acute Control
A
Rapid changes in local vasodilation/vasoconstriction
Occurs in seconds to minutes
2
Q
Describe Long-term Control
A
Increase in sizes/numbers of vessels
Occurs over a period of days, weeks, or months
3
Q
Basic theories of Acute Control
A
Vasodilator Theory
Oxygen (nutrient) lack theory
4
Q
Vasodilator theory
A
Increase Metabolism –> decrease O2 availability –> formation of vasodilators (adenosine, carbon dioxide, adenosine phosphate compounds, histamine, potassium ions, hydrogen ions)
5
Q
Oxygen (nutrient) lack theory
A
Decrease [O2] –> BV relaxation –> Vasodilation
6
Q
Define Vasomotion
A
Cyclical opening and closing or precapillary sphincters
7
Q
Number of precapillary sphincters open at any given time is roughly proportional to:
A
nutritional requirements of tissues
8
Q
Hyperemia - Reactive
A
Tissue blood flow blocked –(unblocked)–> Blood flow increases 4-7x normal
9
Q
Hyperemia - Active
A
When any tissue becomes active, rate of blood flow increases
10
Q
Autoregulation
A
Rapid increase in arterial pressure leads to increased blood flow.
Within minutes, blood flow returns to normal even with elevated pressure.
11
Q
Theories that explain autoregulation
A
Metabolic theory
Myogenic theory
12
Q
Metabolic theory
A
Increase in blood flow –> Too much O2 or nutrients –> Washes out vasodilators
13
Q
Myogenic theory
A
Stretching of vessels –> reactive vasculature constriction
14
Q
Special Acute Blood Flow in the Kidneys
A
Tubuloglomerular feedback: involves the macula densa/juxtaglomerular apparatus
15
Q
Special Acute Blood Flow in the Brain
A
Increase [CO2] and/or [H+] –> cerebral vessel dilation –> washing out of excess CO2/H+
16
Q
Special Acute Blood Flow in the Skin
A
Blood flow linked to body temp.
Sympathetic nerves via CNS
3 ml/min/100 g tissue –> 7-8 L/min for entire body
17
Q
Review endothelial-derived mechanisms for control of tissue blood flow
A
Slides 16 and 17
18
Q
Vasoconstrictors
A
Norepinephrine
Epinephrine
Angiotensis II
Vasopressin
19
Q
Vasodilators
A
Bradykinins
Histamine
20
Q
Angiotensin II normally acts to _______ total peripheral resistance
A
Increase
21
Q
Vasopressin
A
aka ADH
Very powerful vasoconstrictor
Major function is to control body fluid volume
22
Q
Bradykinins
A
Causes both vasodilation and increased capillary permeability
23
Q
Histamine
A
Powerful vasodilator derived from mast cells and basophils
24
Q
Sympathetic System
A
Innervates all vessels except capillaries
Primarily results in VASOCONSTRICTION
25
What is the function of the vasoconstrictor area of the brain?
Transmits continuos signals to BVs:
- continual firing results in sympathetic vasoconstrictor tone
- partial state of contraction of BVs = vasomotor tone
26
What is the function of the vasodilator area of the brain?
Inhibits activity in vasoconstrictor area
27
What is the function of the sensory area of the brain?
Receives signals via Vagus Nerves and Glossopharyngeal Nerves & transmits the signals to the motor areas
28
Higher nervous centers that control the vasomotor centers of the brain:
Reticular substance (RAS)
Hypothalamus
Cerebral Cortex
29
Adrenal Medulla Secretes:
Epinephrine and Norepinephrine
30
Neural Rapid Control of Arterial Pressure Simultaneous Changes:
Constriction of most systemic arteries
Constriction of veins
Increased HR
31
Where are Baroreceptors located?
In Carotid sinuses and aortic sinuses
32
Baroreceptors are stimulated by:
Low arterial pressure
33
Baroreceptors in the carotid sinuses are stimulated by:
Pressure > 60 mmHG
34
Baroreceptors in the aortic sinuses are stimulated by:
Pressure > 30 mmHg
35
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
36
Where are chemoreceptors located?
Carotid bodies in bifurcation of the common carotids and in aortic bodies
37
Chemosensitive cells sensitive to:
lack of O2, CO2 excess, and H+ excess
38
Chemoreceptor signals pass through:
Herring's nerves and vagus nerves
39
Chemoreceptors play an important role in:
respiratory control
40
Where are low pressure receptors located?
In the atria and pulmonary arteries
41
Low pressure receptors play an important role in:
Minimizing arterial pressure changes in response to changes in blood volume
42
Increase in atrial stretch results in:
Reflex dilation of kidney afferent arterioles
Increase in Heart Rate (via CN X)
Signals to hypothalamus --> dec. [ADH]
Atrial natriuretic peptide (ANP) --> kidneys --> inc. [GFR] & dec. Na+ reabsorption
Decrease Na+ reabsorption
43
Arterial Pressure = ?
Cardiac Output x Total Peripheral Resistance
44
Arterial pressure rises when:
Total Peripheral Resistance is acutely increased
45
Normal functioning kidneys return the arterial pressure back to normal within a day or two:
Pressure diuresis
| Pressure natriuresis
46
Primary Hypertension Characteristics
Increased cardiac output
Increased sympathetic nerve activity
Increase in angiotensin II and aldosterone levels
Impairment of renal-pressure natriuresis mechanisms
Inadequate secretion of salt and water
47
Primary hypertension is of ______ origin
unknown, 90-95% of hypertension
48
Major factors of primary hypertension
Weight gain characterized by: increased cardiac output, increased sym. nerve activity, increased angiotensin II and aldosterone levels, impaired renal-pressure natriuresis mechanisms.
Sedentary life style
49
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
50
Renal causes of hypertension:
```
Chronic renal disease
Renal artery stenosis
Renin-producing tumors
Acute glomerulonephritis
Polycystic disease
Renal vasculitis
```
51
Endocrine causes of hypertension:
```
Cushing syndrome
Exogenous hormones
Pheochromocytoma
Acromegaly
Hypothyroidism
Hyperthyroidism
Pregnancy induced
```
52
Cardiovascular causes of hypertension:
```
Coarctation of the aorta
Polyarteritis nodosa
Increased intravascular volume
Rigidity of the aorta
Increased Cardiac Output
```
53
Neurologic causes of hypertension
Psychogenic
Increased intracranial pressure
Sleep apnea
Acute stress
54
Contributing factors to hypertension:
```
Genetic factors
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
```
55
Factors resulting in decreased peripheral resistance (vessel dilation) leading to decreased blood pressure:
```
^ production of NO
^ release of prostacyclin
^ release of kinins
^ in atrionatriuretic peptide (ANP)
Decreased neural factors (beta-adrenergic)
```
56
Factors resulting in decreased cardiac output leading to decreased blood pressure:
Decreased blood volume
Decreased HR
Decreased contractility
57
Factors resulting in increased cardiac output leading to increased blood pressure:
^ HR
^ Contraction
^ Blood Volume (due to aldosterone)
58
Factors resulting in increased peripheral resistance leading to increased blood pressure:
^ angiotensin II
^ catecholamines
^ thromboxane
^ neural factors (alpha-adrenergic)
59
Humoral Vasoconstrictors:
Angiotensin II
Catecholamines
Endothelin
60
Humoral Vasodilators:
Kinins
Prostaglandins
Nitric Oxide
61
Lethal effects of chronic hypertension:
Early heart failure & coronary artery disease
Cerebral infarct
Kidney Failure
62
Atherosclerosis
Type of arteriosclerosis ("hardening of the arteries")
63
Major characteristics of Atherosclerosis
Presence of lesions within the intima of the vessel wall that protrude into the vessel lumen
64
Non-modifiable risk factors of Atherosclerosis:
AGE - risk ^ between 40-60, death rates from ischemic heart disease ^ w/ each decade
GENDER - uncommon in premenopausal women w/o other risk factors, increase after menopause & eventually exceeds men
GENETICS - some mendelian disorders associated w/ atherosclerosis but mostly multifactorial
65
Modifiable risk factors of Atherosclerosis:
Hyperlipidemia (esp. hypercholesterolemia) - major risk factor; high levels of LDL
Hypertension - increases risk of IHD by 60%; most important cause of left ventricular hypertrophy
Cigarette Smoking
Diabetes
66
Other risk factors of atherosclerosis:
```
Inflammation
Hyperhomocystinemia
Metabolic Syndrome
Lipoprotein
Factors affecting hemostasis
Life style: lack of exercise; competitive stressful life style; obesity
```
67
Inflammation
Intimately linked w/ atherosclerotic plaque formation
Correlated with high levels of LDL
C-reactive protein
68
C-reactive protein (CRP)
Major marker for inflammation
Synthesized by liver
Plays important role in opsonizing bacteria and activating complement
69
Hyperhomocystinemia
Inborn error of metabolism
| Associated with premature vascular disease
70
Metabolic Syndrome
Associated with insulin resistance
71
Characteristics of Metabolic Syndrome
```
Obesity (abdominal fat)
Insulin
Fasting hyperglycemia
Increased lipid triglycerides
Decreased HDL levels
Hypertension
```
72
Endothelial injury or dysfunction of any kind:
Results in intimal thickening
| May lead to formation of atheroma in presence of hyperlipidemia
73
Factors related to endothelial dysfunction:
```
Hypertension
Hyperlipidemia
Cigarette smoke
Homocysteine
Infectious agents
Hemodynamic disturbances
Hypercholesterolemia
```
74
Accumulation of lipoproteins (esp. LDL) is the result of:
Chronic hyperlipidemia (esp. hypercholesterolemia)
75
Lipoproteins accumulate in the ____ and are oxidized by oxygen free radicals generated by ______ or _________
intima
macrophages
endothelial cells
76
Oxidized LDL:
Is ingested by macrophages --> foam cells
Stimulates release of growth factors, cytokines, & chemokines
Is toxic to endothelial cells & smooth muscle cells
77
Monocyte adhesion to endothelium:
Endothelial cells express VCAM-1 that bind monocytes & T cells to endothelium
Monocytes transform into macrophages & engulf lipoproteins
T cells stimulate chronic inflammatory response
Activated leukocytes & endothelial cells release factors that promote smooth muscle cell proliferation
78
Smooth muscle proliferation:
Intimal smooth muscle cell proliferation and extracellular matrix deposition converts a fatty streak into a mature atheroma
79
An atheroma consists of:
Cap of smooth muscle cells, macrophages, foam cells, and other extracellular components, overlying a necrotic center composed of cell debris, cholesterol, foam cells, and calcium
80
In the developmental stages of atherosclerosis, the earliest lesions are ____ ______.
Fatty streaks
| Also seen in all children older than 10
81
In the developmental stages of atherosclerosis, atherosclerotic plaques impinge on the lumen of the artery and grossly appear _____ or _____.
White or yellow
82
In the developmental stages of atherosclerosis, plaques progressively enlarge due to:
Cell death & degeneration and synthesis/degradation of extracellular matrix
83
Atherosclerosis Plaques:
Often undergo calcification
| May rupture, ulcerate, or erode
84
Most common arterial sites for atherosclerosis (most involved to least):
```
Lower abdominal aorta
Coronary arteries
Popliteal arteries
Internal carotid arteries
Circle of Willis
```
85
Short term control of arterial pressure:
Via sympathetic nervous system effects on:
- Total peripheral vascular resistance & capacitance
- Cardiac pumping ability
86
Long term control of arterial pressure:
Via multiple nervous & hormonal controls
Via local controls in the kidney that regulate:
- salt & water excretion
87
Relation of kidney output and arterial pressure:
| If Arterial Pressure Increases then:
Increase in urine output --> pressure diuresis
| Increase in sodium output --> pressure natriuresis
88
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
