Control of blood flow Flashcards
What are some acute controls for local blood flow
Rapid changes in local vasodilation/vasoconstriction
How quickly does acute control (rapid changes in local vasodilation/vasoconstriction) occur
seconds to minutes
What are the basic theories behind acute control (rapid changes in local vasodilation/vasoconstriction)
Vasodilator theroy
oxygen (nutrient) lack theory
What is a method of long-term local blood flow control
increase in sizes/numbers of vessels
how long does it take for long-term control (increase in sizes/numbers of vessels take to occur
over a period of days, weeks, or months
What does the vasodilator theory state
when we have an increase in metabolism we will have lower oxygen availability, which leads to the formation of vasodilators
Explain the oxygen (nutrient) lack theory
Low oxygen concentration leads to blood vessel relaxation, which leads to vasodilation. This is because the smooth muscles in the walls of blood vessels require oxygen to remain contracted
What is the definition of Vasomotion
Cyclical opening and closing of precapillary sphincters
Hyperemia can be _____ or _____
reactive, or active
Give an example of reactive hyperemia
Tissue blood flow blocked (from seconds to hours or more), when you unblock the blood flow increases 4-7x normal
Explain the Vasodilator theory
increased metabolism leads to decreased O2 and thus the formation of Vasodilators
Name some Vasodilators (6)
Adenosine Carbon Dioxide Adenosine phosphate compounds Histamine Potassium ions Hydrogen ions
Explain the oxygen (nutrient) lack theory
Decreased Oxygen leads to blood vessel relaxation (because the smooth muscle that constricts around blood vessels needs oxygen to remain contracted) thus leading to vasodilation
What is the definition of Vasomotion
Cyclical opening and closing of precapillary sphincters
The number of precapillary sphincters open at any given time is roughly proportional to what
nutritional requirements of tissues
Vasomotion is a major component to what theory
oxygen (nutrient) theory
Vasomotion and the oxygen (nutrient) theory assume what
that smooth muscles require oxygen to remain contracted
What is hyperemeia
increase in bloodflow that is greater than normal
What are the two forms of hyperemia
reactive and active
What is reactive hyperemia
tissue blood flow is blocked (for seconds to hours or more)
once unblocked you get a blood flow increase of 4-7 times the normal for (seconds, minutes, or hours) it is the bodies attempt to reapy for hte lost oxygen and nutrients during the blockage
What is active hyperemia
When any tissue becomes active, rate of blood flow increases (ex. exercise)
Explain autoregulation
A rapid increase in arterial pressure leads to an increase in blood flow
within minutes, blood flow returns to normal even with elevated pressure
Autoregulation can occur in
any tissue but is more precise in some such as in the brain
What are two views that explain autoregulation
Metabolic theory and Myogenic theory
Explain the metabolic theory for autoregulation
increased blood flow leads to too much oxygen and nutrients which then wash out the vasodilators leading to a constriction of the vessel and a decrease in flow
Explain the myogenic theory for autoregulation
Stretching of the vessel walls leads to reactive vasculature constriction therefore decreasing blood flow
Where are three special acute blood flow control mechanisms found
Kidneys, Brain, and skin
How do the kidneys effect acute blood flow control
Tubuloglomerular feedback: composition of the fluid in the early distal tubule is detected by an epithelial structure of the distal tubule itself called the macular densa, located at the juxtaglomerular apparatus.
When too much fluid filters form the blood through the flomerulus into the tubular system, feedback signals form the macula densa cause constriction of the afferent arterioles, in this way reducing both renal blood flow and glomerular filtration rate back to nearly normal
How does the brain effect acute blood flow control
increase in CO2 and/or H+ leads to cerebral vessel dilation and thus washes out the excess CO2/H+
Explain how the skin has acute blood flow control
Blood flow linked to body temperature, sympathetic nerves via CNS,
3 ml/min/100g tissue in cooler temps can increase to as high as 7-8 L/min for entire body in higher temperatures
Nitric Oxide is released by who
Endothelial cells
Explain endothelial-Derived mechanisms for vasodilation
Endothelial cells release NO which assists in the activation of cGTP to cGMP (in vascular smooth muscle cells), which then activates Protein kinases and dilates the vessel
What is endothelin
27 amino acid peptide; effective in nanogram quanities
released by damaged endothelial cells and results in vasocontriction
What is eNOS
Nitric oxide synthetase
enzyme in endothelial cells used with O2 and L-arginine to produce NO
What is the half life of NO
6 seconds
Humoral Vasoconstriction molecules
Norepiephrine, Epinephrine, Angiotensin II, Vasopressin
What is the function of angiotensin II
Normally acts to increase total peripheral resistance
What is Vasopressin
aka=ADH
very powerful vasoconstrictor
major function is to control body fluid volume
Humoral Vasodilators
Bradykinins, Histamine
What is the function of bradykinins
cause both vasodilation and increased capillary permeability
What is the function of histamine
Powerful vasodilator derived from mast cells and basophils
The sympathetic nervous system innervates all vessels except?
Capillaries
The sympathetic nervous system primarily results in _____
Vasoconstriction
Retrolental fibroplasia
abnormal proliferation of fibrous tissue immediately behind the lens of the eye, leading to blindness.
affected many prematutre babies in the 1950s, owing to the excessive administration of oxygen
What is meant by humoral control of circulation
control by substances secreted or absorbed into the body fluids, such as hormones and locally produced factors.
Epinephrine is normally a vasoconstrictor but can cause mild vasodilation in some areas such as the ___
coronary arteries during increased heart activity
this is because it has a beta-adrenergic receptor stimulatory effect
which is a stronger vasoconstrictor epinephrine or norepinephrine
norepinephrine
As little as one millionth of a gram of angiotensin II can increase the arterial pressure of a human being by
50mm Hg or more
Which is a stronger vasoconstriction ADH or Angiotensin II
ADH
Where is ADH formed
in the hypothalmus
Where is ADH secreted from
posterior pituitary gland
What are the 3 vasomotor centers in the brain called
vasoconstrictor area, vasodilator area, sensory area
Where is the vasoconstrictor area found
in the bilateral anterolateral portions of the upper medulla
What vasomotor center in the brain transmits continuous signals to the blood vessels
Vasoconstrictor area
The partial state o f contraction of blood vessels is referred to as
vasomotor tone
The Vasodilator area is located in what part of the brain
Bilateral in the anterolateral portions of lower medulla
What is the function of the vasodilator area
inhibits activity in vasoconstrictor area thus leading to dilation
Where is the sensory area of the vasomotor center of the brain located
Bilateral in tractus solitarius in posterolateral portion of medulla
The sensory area of the vasomotor center of the brain receives signals from where
vagus nerves (CN X) and Glossopharyngeal nerves (CN IX)
Where are some higher nervous centers that control arterial pressure
Reticular substance (RAS), Hypothalamus, Cerebral Cortex
The lateral and superior portions of the RAS cause what in the smooth muscles around vessels
Excitation
The medial and inferior portions of the RAS have what effect on vessels
They inhibit excitation of smooth muscles around them
The posterolateral portions of the hypothalmus mainly has what effect on vessels
excitation of the smooth muscles around them
The anterior portion of the hypothalmus mainly has what effect on vessels
causes inhibition of smooth muscles around it
Baroreceptors in the internal carotid arteries are stimulated by pressures
Greater than 60 mm Hg
Baroreceptors in the Aorta is stimulated by pressures
greater than 30 mm Hg
The aortic baroreceptors send signals to
CN X and then to the sensory area
Baroreceptors in the internal carotid send signals to the ___ via ____
Sensory area, via Hering’s nerves which then jump onto CN IX
Once the baroreceptors get there signal to the sensory area what happens
it positively acts on Vasodilator area which then inhibits vasocontrictor area
The Adrenal Medulla secretes what
Epinephrine and Norephinephrine
What are three rapid neural controls of arterial pressure
Simultaneous changes of
- constriction of most systemic arteries
- constriction of veins
- Increased heart rate
The neural rapid control of arterial pressure occurs in
seconds
The neural rapid control of arterial pressure is seen during exercise and leads to
increased blood pressure, (accompanied by vasodilation)
is fight or flight (alarm reaction) an example of neural rapid control of arterial pressure
Yes
Baroreceptors are located wher
in interal carotid sinuses and aortic sinus
baroreceptors are stimulated by what
high arterial pressures
The carotid sinus baroreceptors are stimulated by pressures
greater than 60mm Hg
The arotic Baroreceptors are stimulated by pressure
greater than 30 mmHg
Baroreceptors inhibit what
Vasoconstriction center
Baroreceptors excite the
vasodilator center
Signals from the Baroreceptors either cause
increase or decrease in arterial pressure
What is the primary function of Baroreceptors
to reduce the minute by minute variation in arterial pressure to about one third that which would occur if they weren’t present
Baroreceptors work as a pressure _____ system
buffer
Baroreceptors reset every
1 to 2 days
Where are chemoreceptors located
In carotid bodies of bifurcation of the common carotids and in aortic bodies
Chemoreceptors are sensitive to
lack of oxygen, carbon dioxide, and hydrogen ion excess
Signals from chemoreceptors pass from
herring’s nerves and vagus nerves
Chemoreceptors play an important role in what
respiratory control
The atrial reflexes are controlled by
low pressure receptors located in the atria and pulmonary arteries
What is the main function of low pressure receptors in atria and pulmonary arteries
play an important role in minimizing arterial pressure changes in response to changes in blood pressure
Increase in atrial stretch is sensed by low pressure receptors and results in what
reflex dilation of kidney afferent arterioles
increase in heart rate
signals to hypothalamus to decrease ADH secretion
ANP is released and acts on Kidneys to extreme fluid in urine—- increase GFR and decrease NA reabsorption
Atrial pressure is equal to what
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
What is pressure diuresis
effect of increased blood pressure to raise urinary volume excretion
What is pressure natriuresis
rise in sodium excretion that occurs with elevated blood pressure
What are the two methods that kidneys return arterial pressure back to normal in a day or two
Pressure diuresis, Pressure natriuresis
Characteristics of primary HTN
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 HTN is also known as
Essential HTN
Primary HTN is what percentage of HTN
90-95%
Primary HTN has what origin
unknown
What are the major factors of primary HTN
weight gain characterized by
- increased CO
- Increased sympathetic nerve activity
- Increased Angiotensin II and aldosterone levels
- Impaired renal-pressure natriuresis mechanism
sedentary life style
Secondary HTN is second to some other causes like what
Tumor affecting renin-secreting juxtaglomerular cells Renal artery constriction Coarctation of the aorta Preeclampsia Neurogenic HTN Genetic causes
What are some renal causes of HTN
CRD Renal artery stenosis Renin-producing tumor Acute glomerulonephritis polycystic disease renal vasculitis
Endocrine causes of HTN
Cushings syndrom (adrenocortical hyperfunction)
Exogenous hormones (glucoricooids, estrogen)
Pheochromocytoma
Acromegaly
Hypothyroidism (myxedma)
Hyperthyroidism (thyrotoxicosis)
Pregnancy induced
Cardiovascular causes of HTN
Coarctation of the aorta (stenosis of aorta) Polyarteritis nodosa Increased intravascular volume Rigidity of the aorta Increased cardiac output
What is polyarteritis nodosa
systemic vasculitis of small or medium sized muscular arteries
Neurologic causes of HTN
Psychogenic
Increased intracranial pressure
Sleep apnea
Acute Stress
What are some contributing factors to HTN
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
What are some factors resulting in decreased peripheral resistance (vessel dilation) leading to decreased blood pressure
Increased production of NO
Increased release of prostacyclin
Increased release of kinins
Increase in atrionatriuretic peptide (ANP)
Decreased neural factors (Beta-adrenergic)
Factors resulting in decreased cardiac output leading to decreased blood pressure
Decreased blood volume
Decreased heart rate
decreased contractility
Factors resulting in increased cardiac output leading to increased blood pressure
Increased HR
increased contraction
increased blood volume (due to aldosterone)
Factors resulting in increased peripheral resistance leading to increased blood pressure
Increased angiotensin II
Increased catecholamines
Increased Thromboxane
Increased neural factors (alpha adrenergic)
Humoral vasoconstrictors
Angiotensin II
Catecholamines
Endothelin
Humoral vasodilators
Kinins
Prostaglandins
Nitric Oxide
What are three lethal effects of chronic HTN
early heart failure and CAD
Cerebral infarct
Kidney failure
What is atherosclerosis
is a type of arteriosclerosis (hardening of the arteries)
What is the major characteristic of atherosclerosis
presence of lesions within the intimate of the vessel wall that protrude into the vessel lumen
Give 3 non-modifiable (constitutional) risk factors for atherosclerosis
Age, Gender, Genetics
The risk of atherosclerosis increases between the ages of ___ and ___-
40 and 60
The death rates from ischemic heart disease secondary to atherosclerosis increase with each what
decade
Atherosclerosis is uncommon in ______ women without other risk factors
premenopausal
The risk of atherosclerosis increases after ______ in women and eventually _______ that of men
menopause, exceeds
There are some medelian disorders associated with atherosclerosis but mostly _____-
multifactorial
What are four modifiable risk factors for atherosclerosis
Hyperlipidemia, HTN, Cigarette smoking, Diabetes
Hyperlipidemia is a ______ risk factor of atherosclerosis
major
hyperlipidemia is correlated with high levels of ____ (carries cholesterol to peripheral tissues) as opposed to _____ (carries cholesterol to the liver)
LDL, HDL
What is the most important cause of left ventricular hypertrophy
HTN
HTN increases the risk of ischemic heart disease by what
60%
What are 6 other risk factors of atherosclerosis
Inflammation, Hyperhomocystinemia, Metabolic syndrome, Lipoprotein (a), Factors affecting hemostasis,
Life style: lack of exercise, competitive (stressful life style), Obesity
Inflammation in the vessels is intimately linked with what
atherosclerotic plaque formation
What is a major maker for vessel inflammation
C-reactive protein (CPR)
Where is C-reactive protein (CPR) synthesized
Liver
What is the function of C-reactive protein
Plays important role in opsonizing bacteria and activating complement
Inflammation is correlated with high levels of
LDL (carries cholesterol to the peripheral tissues)
Hyperhomocystinemia is what
inborn error of metabolism
associated with premature vascular disease
What is metabolic syndrome
Associated with insulin resistance characteristics: - Obesity ( esp. abdominal fat) - Insulin Resistance - Fasting hyperglycemia - Increased lipid triglycerides - Decreased HDL (carries cholesterol to the liver) levels - Hypertension
What is the pathogenies of Atherosclerosis
Endothelial injury or dysfunction of any kind
- results in intimal thickening
- may lead to formation of atheroma in presence of hyperlipidemia
Accumulation of lipoproteins
Monocyte adhesion to endothelium and then enters intima. It is now a macrophage and engulfs the oxidized lipoprotein, thus forming a foam cells. this leads to the release of growth factors and inflammation.
smooth muscle proliferation
What are some factors related to endothelial dysfunction and atherosclerosis
HTN Hyperlipidemia Cigarette smoke Homocysteine Infectious agents Hemodynamic disturbances Hypercholesterolemia
What is the result of chronic hyperlipidemia
Accumulation of lipoproteins (esp. LDL) thus leading to atherosclerosis
Lipoproteins accumulate in the ____ and are oxidized by oxygen free radicals generated by ___ or ____
intima, macrophages, endothelial cells
Oxidized LDL is ingested by macrophages which become what
Foam cells
Oxidized LDL stimulates the release of ____ , ____, and ___
growth factors, cytokines, and chemokines
Oxidized LDL is toxic to_____ and ________
Endothelial cells and smooth muscle cells
Endothelial cells express _____ adhesion molecules that bind monocytes and T cells to the endothelium
VCAM-1
Endothelial cells express VCAM-1 adhesion moleucules that bind ___ and ___ to endothelium
Moncytes and T cells
When monocytes bind to endothelial cells they transform into ___ and engulf ____
macrophages, lipoproteins
When T-Cells bind to the endothelium they stimulate what
Chronic inflammatory response
Activated leukocytes and endothelial cells release growth factors that promote _________ and lead to atherosclerosis
smooth muscle proliferation
intimal smooth muscle proliferation and extracellular matrix deposition converts a _____ into a ____
fatty streak into a mature atheroma
An atheroma consist of what
cap of smooth muscle cells, macrophages, foam cells (converted macrophages), and other extracellular component, overlying a necrotic center composed of cell debris, cholesterol, foam cells, and calcium
The earliest lesion of atherosclerosis are
fatty streaks: note these are also seen in all children older than 10
Fatty streaks are seen in who
all children older than 10
Describe the developmental stages of atherosclerosis
fatty streaks
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
What are the 5 most common arterial sites for atherosclerosis (most involved to least)
- lower abdominal aorta
- coronary arteries
- Popliteal arteries
- internal carotid arteries
- Circle of Willis
The sympathetic nervous system has short term control on arterial pressure by effecting what
total peripheral vascular resistance and capacitance
Cardiac pumping ability
What are some examples of long term control of arterial pressure
via multiple nervous and hormonal controls
via local controls in kidney that regulate salt and water excretion
what leads to pressure diuresis and pressure natriuresis
increased arterial pressure
The goal of pressure diuresis and pressure natriuresis is what
Return of the arterial pressure always back to the equilibrium point= near infinite feedback gain principle
What is the near infinite feedback gain principle
The kidneys are able to get the arterial pressure almost always back to the equilibrium point. this means that they have little error and are thus close to making an infinite gain when using the gain=corrected/error equation
What are the 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
What are two ways of increasing arterial pressure
the renal output curve is shifted to the right to increase arterial pressure
The salt wan water intake shows that an increase in intake will result in an increase in arterial pressure
what is chronic HTN
one’s mean arterial pressure is greater than the upper range of the accepted normal measure
What is the normal blood pressure and mean
110/70 mean of 90 mmHg
What is hypertensive blood pressure and mean
135/190 and a mean of 110mmHg
What is severe HTN and mean
250/130 and a mean of 150-170mmHg
What are 5 lethal effects of chronic HTN
Early heart failure CAD Heart attack Cerebral infarct Destruction of areas of kidney---> kidney failure---> uremia ---> death
What is uremia
a raised level in the blood of urea and other nitrogenous waste compounds that are normally eliminated by the kidneys
Describe the Renin-Angiotensin system
Decreased arterial pressure—-> kidney, releases renin—-> renin acts on the substrate angiotensinogen (form the liver) thus forming Angiotensin I (has mild vasoconstrictive properties but not enought to cause significant changes in circulatory functions——> ACE (angiotensin converting enzyme released form endothelium in many tissues including the lungs) converts angiotensin I to angiotensin II (which is a strong vasoconstrictor)——> acts acutely within 20 minutes by constricting arteries (thus increasing peripheral resistance) and to a lesser extent constricting veins (thus leading to increased venous return), it also acts directly on the kidneys to increase salt and water reabsorption as well as on the adrenal gland to release aldosterone and thus leads to more sodium and water reabsorption and extened blood pressure control.
What is Renin
a protein enzyme released by the kidneys when the arterial pressure falls too low. it is an enzyme and not a vasoactive substance
Renin is synthesized and stored in an inactive form called ______ in the _________ of the kidney
Prorenin, Juxtaglomerular cells
How long does the renin-angiotensin vasoconstrictor system require to become fully active
20 minutes
The effect of angiotensin to cause renal retention of salt and water can have a powerful effect in promoting what
chronic elevation of the arterial pressure
The renin-angiotensin system is a ______ mechanism that helps maintain the arterial pressure at or near the normal level even when salt intake is increased
automatic feedback
Increased salt intake leads to what
increased extracellular volume—-> increased arterial pressure—-> decreased renin and angiotensin—> decreased renal retention of salt and water—-> Return of extracellular volume almost ot normal —> return of arterial pressure almost to normal
what is the body’s most powerful system for accommodating wide variations in salt intake with minimal changes in arterial pressure
Renin-angiotensin system
Renin-angiotensin system is powerful enough to return the arterial pressure at least ________ within a few minutes after severe hemorrhage
At least haflway back to normal
Explain “one-kidney” Goldblatt hypertension
occurs when one kidney is removed an remaining renal artery of the other kidney is constricted. The immediate effect is greatly reduced pressure in the renal artery beyond the constrictor. Systemic pressure will rise for several days due to a large release of renin. This leads to increase of angiotensin II and aldosterone in the blood. secretion of renin rises to a peak in an hour or so but returns nearly to normal in 5 to 7 days because renal arterial pressure by that time has also risen back to normal, so the kidney is no longer ischemic. The second rise in arterial pressure is caused by the retention of salt and water .
