Vascular Mechanics and regulation

Question 1

Change in Pressure =

Answer 1

CO x R

Question 2

Driving Pressure

Answer 2

The pressure gradient between two points
e.g. for the systemic circulation ∆P = Pa-Pv.
The driving pressure governs blood flow.

Question 3

Transmural Pressure

Answer 3

The pressure across the vessel wall

(inside minus outside)

Question 4

• Hydrostatic Pressure

Answer 4

Dependent on gravity

Question 5

LaPlace Equation

For a thick walled cylinder:

Answer 5

T= (P*r ) /Wall thickness

Question 6

The larger the vessel radius the ____the wall tension required to withstand an
internal pressure

Answer 6

larger

Question 7

Aneurysm

Answer 7

Thinning of vessel wall
 Radius increases
 Wall tension increases
viscous circle!!

Question 8

Hydrostatic pressure: P = ρgh

What is ρgh and units?

Answer 8

ρ = density of the fluid (kg m-3)
g = acceleration due to gravity (9.81 m s-2)
h = distance below the surface (m)
Units – usually mmHg (or kPa), (1 mmHg = 13
mm H2O)

Question 9

Total pressure at a specific point =

Answer 9

hydrostatic pressure + vascular pressure
generated by heart
Thus in large arteries in foot when standing:

Question 10

Intrinsic mechanisms
(autoregulation)
 Distribute blood flow to ?

Answer 10

individual

organs and tissues as needed

Question 11

Extrinsic mechanisms
• Maintain?
• Redistribute blood during ?

Answer 11

mean arterial pressure (MAP)

exercise and
thermoregulation

Question 12

Neural regulation of vascular tone

(resistance) is primarily via ?

Answer 12

the

sympathetic nerves

Question 13

In most cases increased sympathetic

activity increases vascular ?

Answer 13

tone (via

vascular smooth muscle contraction).

Question 14

• NE released from sympathetic

terminals in vasculature binds to the?

Answer 14

α1-adrenoceptors leading to

vasoconstriction

Question 15

A decrease in sympathetic nerve

firing leads to vaso?

Answer 15

dilation

Question 16

Vasoconstriction is in response to ___________release of norepinephrine
acting on _________receptors on
vascular smooth muscle

Answer 16

postganglionic

α1-adrenergic

Question 17

Vasodilation may occur in response to
activation of \_\_\_\_\_\_\_receptors,
e.g. in vasculature in skeletal muscle.
Primarily in response to epinephrine
released from the adrenal \_\_\_\_\_\_\_

Answer 17

β2- adrenergic

medulla

Question 18

The __________are the predominant α-receptor located on

vascular smooth muscle.

Answer 18

α1-adrenoceptors

Question 19

__ released from sympathetic terminals
in vasculature binds to the α1- adrenoceptors
These receptors are linked to _________ receptors that activate ______________
contraction through the IP3 signal transduction pathway and ultimately
vasoconstriction

Answer 19

NE
G-protein

smooth muscle

Question 20

β2-adrenoceptors are mostly found in ???? (also airway smooth
muscle)

Answer 20

skeletal

muscle vasculature

Question 21

β2 -adrenoceptors are More sensitive to ______vs ______

Answer 21

adrenaline

noradrenaline

Question 22

Stimulation of β2-receptors results in?

Answer 22

vasodilation.

Question 23

β2 -adrenoceptors Act via cAMP to inhibit _____light chain kinase, and thus inhibit contraction
Contributes to increase in blood flow during
exercise in response to circulating _______

Answer 23

myosin

adrenaline

Question 24

β2-agonists (activators) e.g.

Answer 24

salbutamol, are useful in

the treatment of asthma (bronchial dilators)

Question 25

Alpha1-adrenoreceptors

Antagonists, e.g.

Answer 25

prazosin (treat high blood pressure) can be useful

in the treatment of severe hypertension

Question 26

Progressive increase in ______ _______ ______with mean arterial pressure

Answer 26

muscle sympathetic

nerve

Question 27

Blood Flow within tissues primarily responds to
changes in ______needs, often at the level of
the precapillary ______

Answer 27

metabolic

sphincters

Question 28

Factors that promote dilation are:

Answer 28

Decreased tissue oxygen levels
 Increased levels of CO2 and H+ (brain)
The generation of lactic acid or other acids by tissue
cells.
The release of adenosine, prostaglandins and nitric
oxide (NO) from endothelial cells.
Rising concentrations of potassium ions or hydrogen
ions in the interstitial fluid.
Chemicals released during local inflammation, including
histamine and NO.
Elevated local temperatures (skin)

Question 29

Reactive hyperaemia

Driven by _______

Answer 29

When blood flow is restored
after a brief occlusion, blood flow rises above pre-occlusion level for a period proportional to the duration of the occlusion.

metabolites

Question 30

Vascular Autoregulation:

Answer 30

Intrinsic capacity to maintain
constant blood flow despite
changes in perfusion (circulatory) pressure.

Question 31

In many tissues (e.g. brain, kidney) blood flow is _______ over a wide range of pressures
Less important in other
vascular beds e.g. cutaneous circulation (skin) and________

Answer 31

near constant

skeletal muscle.

Question 32

Myogenic mechanisms are intrinsic (built-in) to the ______ blood vessels, particularly in
small arteries and _______

Answer 32

smooth muscle

arterioles

Question 33

Autoregulation ensuring flow is constant. Likely due to ______sensitive ion
channels (___) opening,
leading to depolarization.

Answer 33

stretch

Ca2+

Question 34

If the pressure within a myogenic vessel
is suddenly increased, the
vessel responds by _______,
normalizing flow

Answer 34

constricting

FLOW

Question 35

Three unique mechanisms mediate

the CV adjustments:

Answer 35

the arterial
baroreflex, central command, and
the skeletal muscle exercise pressor
reflex.

Question 36

The net effect of BP control is an exercise-induced increase in sympathetic
nerve activity and decrease in
parasympathetic nerve activity that
is actively modulated by the?

Answer 36

arterial

baroreflex.

Question 37

Blood pressure control in exercise downstream effects

Answer 37

Increases in heart rate (HR),
cardiac output (CO), cardiac
contractility, and blood pressure
along with elevations in arterial
resistance and reductions in venous
capacitance