Vascular Physiology 1

Question 1

mean arterial pressure (MAP) - defined

Answer 1

*the average pressure in the vascular system
*note that MAP is not halfway between systolic and diastolic pressures
*this is because MORE TIME IS SPENT IN DIASTOLE than in systole

Question 2

pulse pressure

Answer 2

the difference between the systolic and diastolic pressures (pulse pressure = systolic - diastolic)

Question 3

mean arterial pressure (MAP) - equations

Answer 3

1. MAP = cardiac output x SVR
   OR
2. MAP = 2/3 diastolic BP + 1/3 systolic BP
   OR
3. MAP = diastolic BP + 1/3 pulse pressure

note: pulse pressure = systolic BP - diastolic BP
therefore: MAP = diastolic BP + 1/3(systolic - diastolic)

Question 4

MAP and heart rate

Answer 4

*faster heart rate = more time spent in systole
*results in an increased mean arterial pressure

Question 5

change in pressure = ?

Answer 5

ΔP = Q x R

ΔP: pressure gradient (change in pressure)
Q: flow
R: resistance

Question 6

ΔP = Q x R: relationships

Answer 6

*change in pressure gradient is directly proportional to both flow and resistance (i.e. increased flow leads to increased pressure difference, etc)
*resistance is directly proportional to change in pressure gradient and INVERSE TO FLOW (R = ΔP/Q)
*flow is directly proportional to change in pressure gradient and INVERSE TO RESISTANCE (Q = ΔP/R)

Question 7

ΔP = Q x R related to mean arterial pressure

Answer 7

MAP = cardiac output x systemic vascular resistance

note: resistance can never be measured, only calculated
note: systemic vascular resistance (SVR) is INTERCHANGEABLE WITH total peripheral resistance (TPR)

Question 8

conversion factor from Woods Units to dynes (for systemic vascular resistance)

Answer 8

multiply the calculated resistance (in Woods Units: mmHg*min/L) by 80

note: dynes*s/cm^5 is the unit you are converting to

Question 9

aorta and aging

Answer 9

*as people age, their arteries elongate and become more curvy/twisted; this results in a HIGHER RESISTANCE, which is one reason why our blood pressure gets higher as we age
*additionally, as we age, the aorta becomes STIFFER

Question 10

what is the main principle site of resistance in the CV system

Answer 10

*ARTERIOLES have a very high resistance to flow
*arterioles can selectively constrict or dilate to alter flow to individual organs based on the needs of that organ

Question 11

formula for calculating resistance

Answer 11

R = (8 x viscosity x length) / pi x r^4

recognize that resistance is INVERSELY RELATED to the radius (r) to the 4th power, so a SMALLER diameter/radius of a vessel means MUCH MORE RESISTANCE TO FLOW
*this is relevant because the major way our vascular system modifies flow is through changing resistance, specifically through changing the RADIUS/DIAMETER OF THE ARTERIOLES

Question 12

flow vs velocity

Answer 12

*flow: the amount of blood crossing an area over a period of time (measured in L/min); tells us how MUCH, but not the speed
*velocity: the speed of travel; how far the blood travels over a period of time (measured in cm/s); tells us how FAST, but not how much

Question 13

velocity vs. cross-sectional area

Answer 13

*velocity = flow/area
*when pushing blood across a vessel (or heart valve), if the cross-sectional area gest small, then the velocity has to increase to maintain the same rate of flow!

Question 14

increase in velocity → turbulence

Answer 14

*the greater the velocity, the greater the chance that blood flow will be turbulent
*as the cross-sectional area is reduced from atherosclerotic plaques or stenotic valves, it leads to increased velocity, which can cause turbulent flow
*turbulence causes: audible murmur, audible bruit

Question 15

where is most of the blood in the CV system

Answer 15

*majority is in the systemic circulation, especially in the veins (veins are more compliant than arteries)

Question 16

as we travel through the vascular tree, how do the muscle, elastin, and collagen change?

Answer 16

*muscle: peripheral arteries/arterioles > distal aorta > proximal aorta (muscle content increases)
*elastin: proximal aorta > distal aorta > peripheral arteries (elastin content decreases)
*collagen is consistent in content throughout

Question 17

energetics of blood flow in the aorta

Answer 17

*aortic valve closes at the dicrotic notch
*after aortic valve closure, the energy stored in the stretching of the ascending aortic wall during systole recoils in early diastole
*this propels the blood both to the supra-aortic vessels and the coronary arteries as the dicrotic wave

Question 18

aortic wall stress

Answer 18

*aortic wall stress = (pressure x radius) / (2 x aorta wall thickness)
-as aortic radius increases, the aortic wall stress increases
-as aortic pressure increases, the aortic wall stress increases
-as aortic wall thickness increases, the aortic wall stress DECREASES (and vice versa)

Question 19

aortic wall stress & its clinical manifestations

Answer 19

*in aortic aneurysms, the increased radius increases the wall stress and risk of tearing the intima, which leads to an aortic dissection
*hence, aggressive blood pressure control is used in individuals with aortic aneurysms to prevent risk of aortic dissection

Question 20

arterial wall stress and its clinical manifestations

Answer 20

*in arteries exposed to high blood pressure, the medial wall hypertrophies to alleviate increased wall stress from the excessive pressure
*histologically, this leads to a higher wall thickness to lumen ratio

Question 21

changes in arteriolar constriction/dilation related to changes in resistance

Answer 21

*controlling arteriolar contraction and relaxation is the most important and direct way to increase or decrease systemic vascular resistance
*vasoconstriction → diameter decreased → increased resistance, decreased flow
*vasodilation → diameter increased → decreased resistance, increased flow

Question 22

vascular smooth muscle contraction → vasoconstriction

Answer 22

1) an increase in free intracellular calcium can result from increased flux of calcium into the cell through calcium channels or by release of calcium from internal stores
2) the free calcium binds to CALMODULIN (a special calcium binding protein)
3) calcium-calmodulin activates myosin light chain kinase (MLCK), an enzyme that is capable of phosphorylating myosin light chains (MLC) in the presence of ATP
4) MLC phosphorylation leads to cross-bridge formation between the myosin heads and the actin filaments → VASOCONSTRICTION

Question 23

vascular smooth muscle relaxation → vasodilation

Answer 23

*vascular smooth muscle relaxation occurs when there is reduced phosphorylation of myosin light chain (MLC):
1) reduced release of calcium by the sarcoplasmic reticulum or reduced calcium entry into the cell
2) inhibition of MLCK (myosin light chain kinase) by increased intracellular concentration of cAMP
3) phosphatase-activated MLC dephosphorylation

Question 24

potassium channels in vascular smooth muscles

Answer 24

*as calcium enters the cell, the cell depolarizes (positive charge is entering the cell)
*calcium activates a potassium channel, which starts the repolarization process (positive change leaving the cell)
*for ATP-sensitive K channel, when ATP is abundant, K channel is blocked
*when ATP is scarce (ischemia), the K channel opens and hyperpolarizes the cell (positive charge leaving the cell)
-prevents the voltage-gated calcium channel from opening, which leads to vasodilation and increased blood flow to ischemic tissue

Question 25

increased intra-cellular calcium causes vasoconstriction or vasodilation??

Answer 25

increased calcium → VASOCONSTRICTION

Question 26

decreased intra-cellular calcium causes vasoconstriction or vasodilation??

Answer 26

decreased calcium → VASODILATION

Question 27

baroreceptors

Answer 27

*sensory nerve endings stimulated by changes in blood pressure
*located in: bifurcation of the carotid sinus, aortic arch
*the signal from these locations goes back to the CNS through the glossopharyngeal nerve to modulate the sympathetic and parasympathetic nervous systems
*there are also low-pressure receptors that respond to decreased volume (vena cava, pulmonary veins, veins)

Question 28

how does blood pressure affect nerve firing of baroreceptors

Answer 28

*as the blood pressure increases, the number of impulses sent from the carotid body and aortic arch receptors increase
*at low blood pressure, there are fewer impulses
*at higher blood pressures, the number of impulses sent reaches a maximum

Question 29

sympathetic nervous system directly influences which components of the CV system?

Answer 29

*heart
*arteries
*veins

Question 30

parasympathetic nervous system directly influences which components of the CV system?

Answer 30

*heart (via the vagus nerve)

Question 31

how do the kidneys monitor the CV system

Answer 31

*kidneys detect decreased blood flow
*renin is released when decreased blood flow/pressure are detected

Question 32

influences of the sympathetic nervous system on the CV system

Answer 32

*the sympathetic nervous system responds chiefly when there is DECREASED BLOOD PRESSURE
*decreased blood pressure → less nerve impulses
*CNS stops inhibiting the sympathetic system
*sympathetic system increases activity, mediated through the effects of norepinephrine, epinephrine, and RAS on the heart and vasculature

Question 33

epinephrine receptors

Answer 33

beta 1 = beta 2 > alpha 1
*predominantly beta

Question 34

norepinephrine receptors

Answer 34

alpha 1 ~ beta 1
*predominantly alpha

Question 35

beta 1 receptor → increased cardiac output

Answer 35

*the binding of epinephrine/norepinephrine to beta-1 adrenergic receptor increases:
-contractility
-relaxation
-automaticity/chronotropy
-dromotropy
*by increasing heart rate and stroke volume, beta-1 receptor INCREASES CARDIAC OUTPUT, but has no direct effects on vasculature

Question 36

beta-2 receptor → vasodilation

Answer 36

*beta-2 is predominantly activated by epinephrine
*located in arteries leading to skeletal muscle, cardiac muscle, and liver
*increases cAMP by Gs protein signaling, which then inhibits myosin light chain kinase, which ultimately prevents the myosin-actin cross-bridge from forming
*DECREASES SYSTEMIC VASCULAR RESISTANCE

Question 37

alpha-1 receptor → vasoconstriction

Answer 37

*alpha-1 receptor is predominantly activated by norepinephrine and epinephrine
*located in almost all arteries and veins
*increases smooth muscle contraction by:
-increased calcium release from sarcoplasmic reticulum
-increased Rho kinase deactivates MLCP
*INCREASES SYSTEMIC VASCULAR RESISTANCE

Question 38

renin-angiotension-aldosterone system (RAS) -overview

Answer 38

*much like the aortic and carotid bodies, the kidneys have baroreceptors which detect low blood pressure
*renin is secreted for 3 reasons:
1) SYMPATHETIC STIMULATION (BETA-1) - this is where beta-blockers treat HTN (by decreasing renin release)
2) decreased blood pressure
3) decreased atrial pressure
*in response, renin is released into the blood stream and travels to the liver

Question 39

RAS cascade

Answer 39

1. renin gets released into the bloodstream, where it goes to the liver to enzymatically cleave angiotensinogen into angiotensin 1
2. angiotensin 1 goes to the lungs, where angiotensin-converting enzyme (ACE) converts it into angiotensin 2
3. ACE also serves as a kininase by breaking down bradykinin, which is a vasodilator
4. angiotensin 2 is the major active product of the RAS system → vasoconstriction → increased BP

Question 40

angiotensin-1 AT-1 receptor: vasoconstriction

Answer 40

*AT-1 receptor is activated by angiotensin 2
*located in almost all arteries and veins
*increases smooth muscle contraction by same methods as alpha-1
*INCREASES SYSTEMIC VASCULAR RESISTANCE
*INCREASES PRELOAD by sodium reabsorption in kidneys and venoconstriction
*leads to release of ALDOSTERONE and VASOPRESSIN

Question 41

aldosterone - overview

Answer 41

*released from the adrenal cortex at the behest of angiotensin 2
*also released as extra-cellular potassium rises
*if stretch receptors in atria indicate that the atria are under-filled, aldosterone may be released

Question 42

aldosterone - functions

Answer 42

*aldosterone secretion leads to sodium and water retention through the kidneys
*kidneys secrete potassium and hydrogen ions to exchange it for sodium, which has gotten released in the urine, which is still in the nephron
*EXCRESS SECRETION → HYPOKALEMIA & METABOLIC ACIDOSIS
*blocked by spironolactone

Question 43

vasopressin (anti-diuretic hormone, ADH) - overview

Answer 43

*released for 3 reasons:
1) secretion stimulated by angiotensin 2
2) decreased blood pressure
3) decreased stretch in the atria

Question 44

vasopressin-1 receptor: vasoconstriction

Answer 44

*located in almost all arteries and veins
*increases smooth muscle contraction
*INCREASES SYSTEMIC VASCULAR RESISTANCE (vasoconstriction)
*INCREASES PRELOAD (venoconstriction and increased free water reabsorption in kidney)

Question 45

vasopressin (ADH) and the kidney

Answer 45

*decreases the urine volume to conserve fluid
*causes Aquaporin, a channel for water, to be expressed at the end of the nephron (distal convoluted tubule) to reabsorb water
*INCREASES PRELOAD

Question 46

summary of sympathetic system vascular smooth muscle receptor secondary messengers

Answer 46

*beta 2 receptor: Gs secondary messenger → increased cAMP → vasodilation
*alpha 1 receptor: Gq secondary messenger → increased intra-cellular calcium → vasoconstriction
*angiotensin 2 type 1 receptor: Gq secondary messenger → increased intra-cellular calcium → vasoconstriction
*vasopressin receptor: Gq secondary messenger → increased intra-cellular calcium → vasoconstriction