DR Sherwan Shal

May, 2007

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 ✦ Vessel internal Diameter
✦ Wall thickness
✦ Elasticity
◆ amount of Elastin-stretchability
✦ Contractility
◆ amount of Smooth Muscle
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 ✦Artery -- much elastin & smooth muscle
◆ can expand and recoil
✦ Arteriole-- smooth muscle, no elastin
◆ less pressure related expansion
✦Capillary - single layer of endothelial cells
◆ allows exchange with interstitial fluid
✦Venule -- no elastin or smooth muscle,
◆ but has venous valves
✦Vein --elastin & smooth muscle
◆ affect venous return to heart
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 ✦ = force of blood against vessel wall
✦ Depends on:
◆ volume of blood
◆ compliance (stretchability) of vessel
◆ resistance of vessel to flow
✦ BP would be constant if blood volume entering arteries
= blood volume leaving arteries BUT it isn’t

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 ✦Arteries = transport from heart to body
✦ walls with some muscle & much elastin
✦aorta & other arteries like balloon--> maintain
pressure head till next ventricular contraction
✦ Elastic recoil maintains pressure fluctuations
coming from ventricles

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 ◆Stroke Volume enters artery in Systole.
Only 1/3 of this leaves artery --> arterioles
✦ During Diastole
◆ no more blood enters arteries
◆ but blood continues to leave due to artery elastic recoil
✦Pulse Pressure =
Systolic Pressure - Diastolic Pressure
◆ 120 mmHg - 80 mmHg = 40 mmHg
◆felt as “pulse” indicative of changes in arterial blood
volume
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 ✦ Average pressure driving blood flow
✦ closer to diastolic pressure, not midpoint since
diastole is longer (at rest)
✦ MAP = Diastolic Pr. + 1/3 Pulse Pr.
✦ e.g. MAP = 80 mmHg + 13.3 = 93

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 ✦ Due to their compliance, arteries have low
resistance (recall the elastin?)
✦ thus all arterial pressures ( Systolic, Diastolic,
Pulse & MAP) remain constant thru arterial
tree
✦ Thus, Arterial Blood Pressure useful in providing
good indicator of CV health
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 Flow = Pressure Gradient / Vascular Resistance
✦ flow is directly proportional to pressure gradient
◆ change in pressure along vessel
◆ directly proportional to vessel diameter
✦ flow is inversely proportional to vascular resistance
◆ vascular resistance = friction

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 ✦ Vessel Radius (r)
◆ flow varies directly as 4th power of radius
✦ Vessel Length (L)
◆longer vessel, more frictional surface area
✦Blood Viscosity (n)
◆ frictional properties of cell or molecule
surfaces as they slide over each other
◆ e.g. polycythemia/blood doping/proteins
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 Blood Flow = πr4ΔP / 8nL
r = vessel radius
P = pressure
n = viscosity
L = vessel length ( doesn’t change)

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 ✦ Arterioles flow thru target tissues
✦ Decrease diameter--> Increase resistance
✦ resistance in arteriole Increase BP; this Increase
BP maintains flow direction
◆ pulsatile waves disappear--> BP steady in
arterioles

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 ✦Compared with arteries, arterioles have less
elastin & more smooth muscle.
✦ Resistance accomplished by effects on Smooth
Muscle
✦smooth muscle relaxed = vasodilation (more
blood flow)
✦smooth m contracted = vasoconstriction (less
blood flow)
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 ✦accomplished by changing vessel diameter
✦ Arterioles responsible for over 60% of the total
resistance to flow of the whole circulatory
system
◆called Total Peripheral Resistance

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 ✦Two types of control of vascular tone
1. Intrinsic-
• locally produced substances/conditions
• Chemical or Physical
2. Extrinsic-
• blood-borne regulatory substances not
released locally
• Neural & Hormonal
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 1. Metabolic Products resulting from local metabolically
active tissue
◆ drop in O2
◆ rise in CO2, H+, lactic & carbonic acid
◆ rise in K+ (due to incr. APs)
◆ rise in adenosine (dilates coronary arteries)
◆ increased prostaglandins
◆ change in osmolarity
ALL these indicate need for more O2
----> VASODILATION

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 ✦Vessel endothelial cells secrete regulator substances
(vasoactive chemical mediators)
◆ Nitric Oxide - relaxes smooth m . EDRF = Endothelial-
Derived Relaxing Factor
◆ Endothelin -most potent vasoconstrictor, smooth m.
contraction
◆ other Growth Factors cause angiogenesis (proliferation
of new vessels)
◆ Histamine- relaxes sm. M., but really part of
inflammatory response
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 ✦Heat or Cold
 heat vasodilates, cold vasoconstricts
 environmental or therapeutic

✦ Myogenic response to stretch causes sm. m

contraction, results from stretch-sensitive Ca++
channels--> contraction
◆ resists change occurring w/stretch
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 ✦SNS most important
◆SNS causes arteriole contraction
◆arterioles always under some SNS effect =
“sympathetic tone”
◆thus, can increase or decrease SNS activity to
change arteriole radius
✦Neural (SNS) & Hormonal
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 ✦ Rearrange to:
Δ Pressure = Flow Rate X Resistance
Mean Arterial Pressure = CO X Resistance
Result:
1. SNS arterial stimulation increases
resistance
2. downstream (arteriole--> capillary) blood
flow to the tissue is decreased
3. upstream (arterial) pressure is elevating
E.g. dam in river

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 ✦ Thus SNS maintains the mean driving pressure
(MAP) to all organs (except brain) , but individual
organs control local flow
✦ intrinsic vasodilation factors can locally override SNS
effect
✦Skeletal & Cardiac M
◆ most sensitive to local factors
◆ greatest need for dramatic changes in blood supply due
to activity and buildup of metabolic products
✦ SNS effects on heart itself increase both HR and SV
(increased venous return)-->
✦ Thus, heart overcomes weaker SNS vasoconstrictor
effects
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 ✦Little PNS innervation of vessels
✦ penile & clitoral blood flow controlled by
PNS
✦Require rapid & diffuse vasodilation for
erection
✦ mechanism via NO synthesis & release
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✦ Adrenal Medulla releases Epinephrine during
STRESS
◆ Epi binds to both α and Β-2 adrenergic
◆ α−binding reinforces SNS vasoconstriction
◆ But Β-2 adrenergic receptors --> vasodilation
✦ B-2 receptors ONLY found in smooth muscle of
◆ Heart, Skeletal muscle & liver
◆ facilitates ability to mobilise energy during stress
(flight or fight) response
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 ✦ Vasopressin (hypothalamic)
✦ Angiotensin II (kidney)
✦ both vasoconstrictors
✦ impt in regulation of water & salt balance via
controlling BP
✦ impt during hemorrhage in trying to maintain
plasma volume & osmolarity
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 Total CO can remain constant, but % CO delivered to
each tissue varies
✦Flow to tissue regulated at 2 points
3. Arterioles
• Controlled through Intrinsic (Local) & Extrinsic factors
4. Capillaries
• Controlled by cuffs of smooth muscle called precapillary
sphincters
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 ✦ In skin -shunts to cut flow thru cap beds (arteriovenous
anastomoses)
✦ some capillary beds connected by Metarterioles betw’n
arteriole & venule
✦these asst’ed with spiraling smooth muscle called
Precapillary sphincters
◆control opening to bed
✦ at rest only 10% PC sphincters open
✦ flow through cap bed depends on metabolic activity
of tissue
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