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74 Cards in this Set
- Front
- Back
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How does increased arterial resistance affect cappillary pressure?
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decreases it but increases the pressure gradient as a result favoring flow
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What is the difference between basal tone and resting tone?
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Basal tone is the state of partial contraction of vessels due to intrinsic properties of walls independent of input
Resting tone is the nomal tone that is normally slighltly more sympathetically tonic tha the basal tone |
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Summarize the difference between active constriction and passive constriction?
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Active constriction is the constriction of a vessel due to neural or metabolic input. Passive constriction is the constriction of a vessel after a preceeding period of active vasodialation. Concept is same for active\passive vasodialation
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What is the effect of adding adenosine to a vessel? SNS via a1 receptor?
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Active vasodialation
Active vasoconstriction |
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What is active hyperemia?
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When increase in metabolic activity produces increases local levels of metabolites(ie CO2) which signal local vasodialation
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What are some examples of vasodialator metabolites; gases and metabolic by-products?
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Gases: PO2, CO2
Metabolites: K+, PO4, lactic acid, prostaglandins, H+, adenosine, NO, increased osmolarity |
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Explain reactive hyperemia?
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This is when an occlusion decreases Bf to a tissue causing myogenic vasodialation and metabolite increase as in active hyperemia so that when the occlusion is removed blood rushes to ischemic area, arteriole much wider than normal
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What is an example of normal physiological reactive hyperemia occlusion?
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Muscle contraction cutting off blood flow
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What are 4 tissues that can autoregulate?
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Heart, brain , kidneys, muscle
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What is autoregulation?
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Concept that a tissue can regulate BP within itself independent of neural or metabolic input, solely based on BP
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What is the fuction of autoregulation?
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To maintain constant blood flow despite changes in blood pressure
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What is the hypothesized cause for autoregulation mechanism?
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No one really knows but it is thought that myogenic activity is responsible
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Where is vasopressin released and what effect does it have on circulation?
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From pituitary>>>Vasoconstriction, water retention(anti-diuretic hormone)
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Where is angiotensin II released and what effect does it have on circulation?
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From angiotensin I, vasoconstriciton
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Where is atrial natriuretic peptide released and what effect does it have on circulation?
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From atria, vasodialator, counteracts hypervolemia(low blood volume)
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Where is sympathetic innvation density high? Low
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High in skin and skeletal muscle vessels
Low in coronary,pulmonary, and cerebral tissues(most control is metabolic) |
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How does sympathetic stimulation via catecholamines inhibit GI function but increase blood to muscles?
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Epinephrine has reciprocal effects in the 2 locations
a1 receptors in GI cause vasoconstricition B2 receptors in Muscles cause vasodialation |
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What are the intrinsic factors that affect vasculature tone?
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Active\reactive hyperemia and autoregulation
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If the GI tract is sympathetically stimulated via a1(vasoconstricted) what are the 2 ways that this can be reversed?
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Overcoming signal via reactive hyperemia from metabolite accumulation or withdrawl of sympathetic stimulation=passive vasodialation
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WHat receptor is utilized by sympathetic and parasympathetic cholinergic receptors?
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M3
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Where does the sympathetic nervous system cause vasodialation via M3 cholinergic receptors?
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skeletal muscle small cappillary beds by relaxing precapillary sphincters
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Where does the parasympathetic nervous system cause vasodialation via M3 cholinergic receptors?Strong or weak effects?
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genetalia, cerebral, coronary small cappillary bed
Effects are weak. These tissues mostly under metabolic control |
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how are precappillary sphincters different from smooth muscle?
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Precapillary sphincters are the gate keepers to metarterioles and are NOT sensetive to sympathetic input, only metabolic
Smooth muscle on arteriolar resistance vessels is sensitive to both |
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What is the stimulus for activation of renin angiotensin system?
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Decreased MAP or extracellular volume
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What is the receptor for angiotensin II in resistance vessel smooth muscle?
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AT1
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What are the effects of an activated Renin-angiotensin system?
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Increase Na and water resorbtion at kidneys, vasoconstriction, vasopressin release(anti-diuretic hormne)
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Where is vasopressin released from?
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posterior pituitary
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What is vasopressin's receptor?
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V1
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What is the stimulation for vasopressin release?
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rising plasma osmolarity, falling bp
Combats both with fluid uptake |
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How does decreased water intake affect ADH(vasopressin) levels in the blood?
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Increases
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How does increasing blood pressure affect ADH(vasopressin) levels in the blood?
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Decreased levels
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What are the 2 forms of natriuretic peptides and where are they released?
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ANP-atria and Brain Natriuretic Peptide-ventricular myocytes
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What stimulated ANP\BNP release?
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Atrial streching or ventricular pressure\overload
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What is the target of ANP and what is its receptor and bichemical effect?
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Vascular Smooth muscle and kidneys, receptor =ANP(a\b) receptors
stimulates gyuanyl cyclase activity which increases cGMP and causes vasodialation and increases Na and water excretion of the kidneys |
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What are the effects of epinephrine via a1\a2 and B2 receptors? Tissues where receptor are?
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a1\a2 causes vasoconstriction(high concentrations)
Most tissues B2 vasodialation- skeletal \heart |
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Why is the effect of epinephrine very potent in skeletal muscle?
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Becuase their is a high density of B2 receptors with high affinity for epinephrine
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What are the forms of neural\hormonal control primarily involved in control of blood flow?
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Neural=sympathetics
Hormonal=angiotensin\renin, epinephrine, vasopressin, ANP |
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What effect does parasympathetic stimulation have on the systemic resistance control?
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None
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Why is the effect of epinephrine very potent in skeletal muscle?
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Becuase their is a high density of B2 receptors with high affinity for epinephrine
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What are the forms of neural\hormonal control of blood flow?
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Neural=sympathetics
Hormonal=angiotensin\renin, epinephrine, vasopressin, ANP |
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What effect does parasympathetic stimulation have on the systemic resistance control?
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Vasodilation via M2 receptors in the heart and M3 in cerebral, coronary, genital tissues
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What signal's NO release and where is it released?
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From endothelial lining cells as a result of shear stress from increased flow or from neurotransmitters that increase endothelial intracellular calcium
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How does NO affect vasodialation?
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Diffuses into vasculature smooth muscle and binds soluble guanyl cyclase and activating it>>> inc cGMP leading to smooth muscle relaxation
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What is EDHF and how does it affect vasculature smooth muscle?
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Endothelial derived hyperpolarizing factor- factors that hyperpolarize SM membrane causing relaxation
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What are the 4 endothelium mediated factors that affect vascular resistance?
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PGI2(prostacylin), NO, EDHF=Vasodialation
Endothelin(ET 1-3 using ET receptors)=Vasoconstriction |
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How does prostacylin act to cause vasodialation
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Increases cAMP and decreases platelet aggrigation
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What signal's NO release and where is it released?
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From endothelial lining cells as a result of shear stress from increased flow or from neurotransmitters that increase endothelial intracellular calcium
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How does NO affect vasodialation?
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Diffuses into vasculature smooth muscle and binds soluble guanyl cyclase and activating it>>> inc cGMP leading to smooth muscle relaxation
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What is EDHF and how does it affect vasculature smooth muscle?
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Endothelial derived hyperpolarizing factor- factors that hyperpolarize SM membrane causing relaxation
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What are the 7 endothelium mediated factors that affect vascular resistance?
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PGI2(prostacylin), NO, EDHF,Kinins, Histamines=Vasodialation
"Open up Pff HEK NO" Endothelin(ET 1-3 using ET receptors),prostaglandins=Vasoconstriction |
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How does prostacylin act to cause vasodialation
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Increases cAMP and decreases platelet aggrigation
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What is the most active vasoconstricting substance known? How does it work?
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Endothelin binds to ET receptors usually in response to vessel streching
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What is the most active vasoconstricting substance known? How does it work?
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Endothelin binds to ET receptors usually in response to vessel streching
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What are 2 kinins and what effects do they have on blood flow?
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bradykinin and kalladin. vasoconstriction in arterioles but ALSO dialaton of veins
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How are the vasodialating effects of histamine caused?
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Via H1 receptors on endothelial cells causing NO release
and H2 receptors on smooth muscle cells which increase cAMP |
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What are 2 kinins and what effects do they have on blood flow?
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bradykinin and kalladin. vasoconstriction in arterioles but ALSO dialaton of veins
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How are the vasodialating effects of histamine caused?
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Via H1 receptors on endothelial cells causing NO release
and H2 receptors on smooth muscle cells which increase cAMP |
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What effect does increase cAMP of cGMP have on smooth muscle cells?
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relaxation>>vasodialation
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How are endothelial lining cells arranged around vessels to allow effecient diffusion to interstitium?
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single layer with water filled pores
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How does histamine act on endothelial lining pores?
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Widens them to increase vasculature permeability
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Why do precappillary sphincters adjust cappillary flow ?
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To allow more perfusion to more of the cappillary beds therby increasing the exchange of metabolites during increased metabolic demand
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What are the 4 forces that drive fluid into or out of the cappillaries to the interstitium?
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-Cappillary blood pressure(Pc)=force exerted by blood on walls
-Plasma colloid osmotic pressure(πp)=pressure pulling interstitial fluid in due to osmotic effect of cappillary proteins -Interstitial fluid hydrostatic pressure(Pif)- fluid pressure of interstitium in to cappillary -Interstitial fluid colloid pressure(πIF)- osmotic pressure exerted by proteins in interstitium |
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What are the 2 major driving forces for fluid movement in cappillaries?
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Cappillary blood pressure and plasma colloid pressure
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How does Cappillary blood pressure change from the arteriole side to the venous side of cappillary beds?
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It starts at about 37mmHg and decreases to about 17mmHg
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Does πp(plasma colloid osmotic pressure) change from the arteriole side to the venous side of capillary beds?
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Not in healthy vasculature, remains at about 25mmHg inward
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What is the standard value of plasma colloid osmotic pressure?
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25 mmHg
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What causes Interstitial colloid osmotic pressure? Is it a major force?
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proteins that leak out of the capillaries and exert an outward osmotic force on capillaries. Not major, usually 0
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When does interstitial colloid osmotic pressure become significant?
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In the situation of injury when proteins leak out of capillaries in response to histamines
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How do you determine net filtration across entire capillary beds?
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First find net inward\outward flows in the arteriolar end then the venous end the find the net.
Use: Net exchange pressure = (PC + πIF) – (πP + PIF)=outward forces-inward forces |
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What are the outward forces affecting capillary fluid movement? inward forces?
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Pc=Capillary blood pressure
πIF=interstital colloid osmotic pressure πP=Plasma colloid osmotic pressure Pif=Interstitial hydrostatic pressure |
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What type of fluid movement usually occurs at the arteroile end and then the venous end of capillary beds?
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Art=filtration
ven=reabsorbtion |
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What happens to sacrum/lumbar when you inhale
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Sacrum extend (posterior), lumbar flex
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If normal net bulk flow is outward at 2mmHg then why doesn't fluid accumulate in the interstitium?
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FLuid is taken up by the lymph vessels
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What are 4 instances where edema results due to interstitial fluid accumulation?
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Reduced plasma proteins, increased venous pressure(CHF), increased capillary permeability, lymph blockage
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