Blake_Physio_11_Control of Blood Flow Flashcards
Acute control of Blood Flow: (3)
- Rapid changes in local vasodilation/vasoconstriction
- Occurs in seconds to minutes
- Basic theories:
- Vasodilator theory
- Oxygen (nutrient) lack theory
Long-term control of local blood flow: (2)
- Increase in size/numbers of vessels
- Occurs over a period of days, weeks, or months
Acute control of blood flow:
Vasodilator Theory
- Increased Metabolism
- Decreases O2 availability
- Forms Vasodilators
- Adenosine
- CO2
- Adenosine phosphate compounds
- Histamine
- K+
- H+
Acute control of blood flow:
Oxigen/Nutrient lack theory
- Decreased O2
- Blood Vessel Relaxation
- Vasodilation
Define Vasomotion:
Cyclical opening and closing of precapillary sphincters
Hyperemia
- Reactive:
- Tissue blood flow blocked
- When unblocked -> blood flow increases 4-7x norm
- Active
- When any tissue becomes active, rate of blood flow increases
Autoregulation of Blood Flow:
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 of blood flow:
Metabolic Theory
Myogenic Theory
Metabolic Theory of blood flow Autoregulation:
- Increase in blood flow
- too much oxygen or nutrients
- Washes out vasodilators
Myogenic theory of blood flow autoregulation:
- Stretching of vessels
- reactive vasculature constriction
Special acute Blood flow control mechanisms (3)
Kidneys
Brain
Skin
How do kidneys control acute blood flow?
- Tubologlomerular feedback:
- Involves the maclula densa/juxtaglomerular apparatus
How dow the brain control acute blood flow?
- [CO2] increases and/or [H+] inceases
- cerebral vessel dilation
- washing out of excess [CO2]/[H+]
How does the skin regulate acute blood flow?
- Blood flow is linked to body Temp
- Sympathetic nerves via CNS
- 3ml/min/100g tissue -> 7-8L/min for entire body
How do Endothelial Cells control tissue blood flow?
- Healthy Endothelial Cells export NO
- NO dephosphorylates cGTP to cGMP
- cGMP activates protein Kinases
- Vasodilation
Humoral Circulation Control
Vasoconstriction
Vasodilation
Vasoconstrictive hormones
- Norepinephrine
- Epinephrine
- Angiotensin II (increases total peripheral resistance)
- Vasopressin (aka: ADH)
Vasodilating Hormones
Bradykinins
Histamine
How does the sympathetic system control vasodilation?
- Vasoconstrictor area of upper medulla transmits a continuous signal to blood vessels resulting in continually, partially contraction of blood vessels = vasomotor tone
- Vasodilator area (bilateral in the anterolateral portions of lower medulla) inhibits the activity of the vasoconstrictor area
Sensory area of vasomotor center of brain
- Bilateral in tractus solitarius in posterolateral portion of medulla
- Receives signals via:
- Vagus Nerve (CN X)
- Glossopharyngeal Nerve (CN IX)
- Controlled by higher nervous centers:
- Reticular Substance (RAS)
- Hypothalamus
- Cerebral Cortex
How does the Adreanal Medulla affect vasomotion?
secretes epinephrine and norepinephrine
Neural Rapid Control of Arterial Pressure: (4)
- Simultaneous Changes
- Constriction of most systemic arteries
- Constriction of veins
- Increased heart rate
- Rapid response (w/in seconds)
- Increased blood pressure during exercise (accompanied by vasodilation)
- Alarm reaction (fight or flight)
Where are baroreceptors located?
Carotid sinuses and aortic sinus
How are Baroreceptors stimulated? (5)
- Stimulated by low arterial pressures
- carotid sinuses are stimulated by pressure >60mmHg
- Aortic sinus is stimulated by pressure >30mmHg
- CN X, CN IX (via small Herring’s nerves)
- RAS
- Hypothalamus
- Cerebral Cortex
Signals from baroreceptors do the following 4 things:
- 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
Where are Chemoreceptors located?
carotid bodies in bifurcation of the common carotids and in aortic bodies
what do chemoreceptors sense?
lack of oxygen, excess carbon dioxide, excess hydrogen ions
How do signals from chemoreceptors pass to the brain?
Herring’s nerves to vagus (CN X)
what is the most important role for chemoreceptors?
respiratory control
What are 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 -> increases [ADH]
- Atrial natriuretic peptide (ANP) -> kidneys
- increased GFR (glomerular filtration rate)
- decreased reabsorption of Na+
Arterial pressure and kidneys:
- Arterial pressure =
- Arterial pressure rises when____
- How do normal functioning kidneys regulate arterial pressure?
- arterial pressure = cardiac output * total peripheral resistance
- Arterial presure rises when total peripheral resistance is increased
- Normal functioning kidneys return arterial pressure back to normal w/in a day or two
- pressure diuresis
- pressure natriuresis
pressure diuresis
urinary excretion of water in order to reduce arterial pressure
pressure natriuresis
urinary excretion of sodium in order to reduce arterial pressure
What are the 5 characteristics of primary hypertension?
- Increased Cardiac output
- increased sympathetic nerve activity
- increased angiotensin II and aldosterone levels
- Impairment of renal-pressure natriuresis mechanisms
- Inadequate secretion of salt and water
What are the 2 major factors of primary hypertension?
- Weight gain
- Sedentary life style
What are the major causes of secondary hypertension? (6)
- Tumor affecting renin-secreting juxtaglomerular cells
- Renal artery constriction
- Coarctation (narrowing) of the aorta
- preclampsia
- neurogenic hypertension
- genetic causes
What are the Renal Causes of Hypertension?
- Chronic renal diseas
- Renal artery stenosis
- Renin-producing tumors
- Acute Glomerulonephritis
- Polycystic disease
- Renal Vasculitus
What are the Endocrine causes of Hyertension? (7)
- Cushing syndrome (adrenocortical hyperfunction)
- Exogenous hormones (glucocorticoids, estrogen)
- Pheochromocytoma
- Acromegaly
- Hypothyroidism (myxedema)
- Hyperthyroidism (thyrotoxicosis)
- Pregnancy induced
What are the Cardiovascular causes of hypertension? (5)
- Coarctation of teh aorta
- polyateritis nodosa
- increased intravascular volume
- Rigidity of the aorta
- Increased cardiac output (usually an outcome of other cause)
What are the neurological causes of hypertension? (4)
- Psychogenic
- Increased Intracranial pressure
- Sleep Apnea
- Acute Stress
What are the contributing factors in Hypertension? (8)
- Genetic
- multifactorial
- single-gene disorders that alter Na+ reabsorp.
- Variants in the renin-angiotensis system
- Lifestyle
- stress
- obesity
- smoking
- inactivity
- heavy dietary sodium
Factors resulting in decreased peripheral resistance leading to decreased blood pressure: (5)
- Increased production of NO
- increased release of prostacyclin
- increased release of kinins
- increase in atrionatriuretic peptide (ANP)
- Decreased neural factors (ß-adrenergic)
Factors resulting in decreased cardiac output leading to decreased blood pressure:
- Decreased blood volume
- Decreased heart rate
- Decrease contractility
Factors resulting in INCREASED cardiac output leading to increased blood pressure: (3)
- Increased heart rate
- increased contraction
- increased blood volume (aldosterone)
Factors resulting in increased peripheral resistance leading to increased blood pressure: (4)
- Increased angiotensin II
- Increased catecholamines
- increased thromboxane
- Increased Neural factors (a-adrenergic)
3 Humoral Vasoconstrictors:
Angiotensin II
Catecholamines
Endothelin
3 Humoral vasodilators:
Kinins
Prostaglandins
Nitric Oxide
Atherosclerosis (2)
- a type of arteriosclerosis (hardening of the arteries)
- Presence of lesions within the intima of the vessel wall that protrude into the vessel lumen
Non-modifiable risk factors for Atherosclerosis:
Age
Gender
Genetics
Modifiable risk factors for atherosclerosis:
hyperlipidemia
hypertension
smoking
diabetes
Other risk factors for atheroclerosis (6)
- Inflamation
- Hyperhomocystenemia
- Metabolic sydrome
- Lipoprotein (a)
- Factors affecting hemostasis)
- life-style
Pathogenesis of Atherosclerosis:
Endothelial injury or dysfunction: (3)
- Intimal thickening
- Formation of atheroma in presence of hyperlipidemia
- Factors:
- hypertension
- hyperlipidemia
- cigarette smoke
- homocysteine
- infectious agents
- hemodynamic disturbances
Pathogenesis of Artherosclerosis:
Accumulation of Lipo proteins (esp LDL): (5)
- Result of chronic hyperlipidemia
- Lipoproteins accumulate in intima and are oxidised by free radicals generated by macrophages or endothelium
- Oxidised LDL is injested by macrophages which become foam cells
- Oxidised LDL stimulates release of GFs: cytokines and chemokines
- Oxidized LDL is toxic to endothelial cells and smooth muscle
Pathogenesis of atherosclerosis
Monocyte adhesion to endothelium: (4)
- Endothelial cells express VCAM-1 adhesion molecules to bind monocytes and T-cells
- Monocytes transform into macrophages and engulf lipoprotiens
- T-cells stimulate a chronic inflammatory response
- Activated leukocytes and endothelial cells release GFs to promote smooth muscle proliferation
Pathogenesis of atherosclerosis
Smooth muscle proliferation:
Intimal smooth muscle cell proliferation and extracellular matrix deposition converts a fatty streak into a mature atheroma
Atheroma Morphology
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
Developmental stages of atherosclerosis: (5)
- Fatty streaks - even in children >10
- Atherosclerotic plaques - impinge on the lumen of the artery and grossly appear white or yellow
- Enlarged plaques - due to cell death and degeneration and synthesis/degradation of EC matrix
- calcified plaques
- Ruptured, ulcerated, or erroded plaques
Most common sites for atherosclerosis (5)
- Lower abdominal aorta
- coronary arteries
- popliteal arteries
- internal carotid
- circle of Willis
Short term control of arterial pressure:
Sympathetic nervous system effects on
- total peripheral vasculare resistance and capacitance
- Cardiac pumping
Long term control of arterial pressure:
- Multiple nervous and hormonal controls
- Local controls in the kidney that regulate salt and water excretion
7 Steps by which increasing EC fluid volume increases arterial pressure
- Increased EC fluid volume
- Increased blood volume
- Increased mean circulatory filling pressure
- Increased venous return of blood to the heart
- Increased cardiac output
- autoregulation
- increased total peripheral resistance
- increased arterial pressure
- increased urine output
- decreased EC fluid vollume (negative feedback)
Define Chronic Hypertension:
- Normal:
- Hypertensive:
- Severe Hypertsnsive:
- One’s mean arterial pressure is greater than the upper range of accepted normal pressure
- Normal: 90 mmHg (110/70)
- Hyper: 110mmHg (135/90)
- Severe: 150-170mmHg (180+/120)
Renin-agiotensin vasoconstrictor mechanism: (6)
- Decreased arterial pressure
- Renin (kidney)
- Renin substrate (angiotensinogen)
- Angiotensin I (ACE: agiotensin converting enzyme; lung)
-
Agiontensin II (inactivated by angiotensinase)
- Atrial natriuretic peptide = Vasoconstriction
- Aldosterone (Adrenal gland) = renal retention of salt and water
- Increased arterial pressure (negative feedback)
Return of arterial pressure to almost normal by renin-angiotensin system following increased salt intake (7)
- Increased salt intake
- Increased EC fluid volume
- Increased arterial pressure
- Decreased Renin and Angiotensin
- Decreased renal retension of Na+ and H2O
- Return of EC volume almost to normal
- Return of arterial pressure to almost normal
