Download Chapter 9b

Plasma = 55% of whole blood
Platelets
“Buffy coat”
<1%
White blood cells
Packed cell
volume, or
hematocrit
Red blood cells =
45% of whole blood
Fig. 9-3, p.361
Platelet
Adenosine
diphosphate
(ADP)
Vessel
lumen
Prostacyclin Inhibits platelet
and nitric acid aggregation
Prostacyclin
and nitric acid
Normal endothelium
Vessel
wall
Aggregating
platelet plug
Normal endothelium
Exposed collagen
at site of
vessel injury
Collagen
Fig. 9-9, p.368
Fig. 9-11, p.369
Goals
• To describe the general structure of blood vessel walls.
• To compare and contrast the types of blood vessels.
• To relate the blood pressure in the various parts of the vascular
system to differences in blood vessel structure.
Peripheral Circulation
•
•
•
•
Arteries
Arterioles
Capillaries
Veins
• Role is to direct
the flow of blood
from the heart to
the capillaries,
and back to the
heart.
Arteries
• Elastic arteries:
– Walls of smooth muscle and elastin.
– Expand when the pressure of the blood rises.
– Acts as recoil system when ventricles relax.
• Muscular arteries:
– Are less elastic and have a thicker layer of
smooth muscle.
• Arterioles:
-Contain highest % smooth muscle.
-Greatest pressure drop.
-Greatest resistance to flow.
Capillaries
• Capillaries consist of only a thin tunica intima or endothelium.
• Most capillaries are arranged in capillary beds.
• Thinness allows exchange of materials between blood and tissues.
Capillaries
•
•
•
•
Smallest blood vessels.
1 endothelial cell thick.
Provide direct access to cells.
Permits exchange of nutrients and wastes.
The velocity of
flow at any point in
the circulation is
not related to the
proximity of the
heart, but to the
total cross-sectional
area of that part of
the circulation.
Venules
Veins
• Venules:
– Formed when capillaries unite.
– Very porous.
• Veins:
– Little smooth muscle or elastin.
– Capacitance vessels (blood reservoirs).
– Contain 1-way valves ensure blood flow to the
heart.
Summary
1. Of the three types of vessels, arteries have the
thickest tunica media (allowing stretch/recoil and
vasoconstriction), veins have relatively thick
tunica adventitia, and capillaries are the thinnest
(allowing exchange of materials.)
2. Blood pressure varies in different parts of the
vascular system. At least part of this variation
reflects vessel structure. Structural adaptations
of veins assist in returning blood to the heart.
Sources of Peripheral Resistance
• Three main sources of peripheral resistance:
1. blood vessel diameter
2. blood viscosity
3. total vessel length
Factors Affecting Blood Pressure
Peripheral Resistance
Blood
Vessel
Diameter
Blood
Viscosity
Total
Vessel
Length
Vessel Elasticity
Blood Volume
Cardiac Output
Total Blood Vessel Length Affects Peripheral Resistance
•Increased fatty tissue requires more blood vessels to
service it and adds to the total vessel length in the body.
•The longer the total vessel length, the greater the
resistance encountered, and the greater the blood pressure.
Blood Pressure Regulation
1. short-term mechanisms, which
regulate blood vessel diameter, heart
rate and contractility
2. long-term mechanisms, which
regulate blood volume
Long-Term Regulation of Low Blood Pressure
• Long-term regulation of blood pressure is primarily
accomplished by altering blood volume.
• The loss of blood through hemorrhage, accident, or
donating a pint of blood will lower blood pressure and
trigger processes to restore blood volume and therefore
blood pressure back to normal.
• Long-term regulatory processes promote the
conservation of body fluids via renal mechanisms and
stimulate intake of water to normalize blood volume and
blood pressures.
Kidney
Juxtaglomerular Cells
• Juxtaglomerular cells
in the kidney monitor
alterations in the blood
pressure. If blood
pressure falls too low,
these specialized cells
release the enzyme renin
into the bloodstream.
Step 1: Renin-Angiotensin Mechanism:
angiotensinogen
renin
angiotensin I
As renin travels through the bloodstream, it binds to an
inactive plasma protein, angiotensinogen, activating it
into angiotensin I.
Step 2: Conversion of Angiotensin I
Converting Angiotensin I to Angiotensin
II: As angiotensin I passes through the
lung capillaries, an enzyme in the lungs
converts angiotensin I to angiotensin II.
angiotensin I enzyme
angiotensin II
Step 3: Angiotensin II Stimulates
Aldosterone Release: Angiotensin II continues
through the bloodstream until it reaches the adrenal
gland.
Here it stimulates the cells of the adrenal cortex to
release the hormone aldosterone.
Angiotensin II as a Vasoconstrictor
• A secondary effect is that angiotensin II is a vasoconstrictor
and therefore raises blood pressure in the body's arterioles
Aldosterone Mechanism
• Long-Term Regulation: The target organ for aldosterone is the
kidney. Here aldosterone promotes increased reabsorption of
sodium from the kidney tubules.
• As sodium moves into the bloodstream, water follows. The
reabsorbed water increases the blood volume and therefore the
blood pressure.
Long-Term Effect of Osmolarity on BP
antidiuretic hormone (ADH).
Distal Tubule
ADH
Long-Term Effect of Osmolarity on BP
• the posterior pituitary to release
antidiuretic hormone (ADH).
Short-Term Effect of Osmolarity on
BP
• excitation of the thirst center in the
hypothalamus, stimulates the individual
to drink more water.
Summary
• In the short-term, rising blood pressure stimulates
increased parasympathetic activity, which leads to
reduced heart rate, vasodilation and lower blood
pressure.
• Falling blood pressure stimulates increased
sympathetic activity, which leads to increased heart rate,
contractility, vasoconstriction, and blood pressure.
• Long-term blood pressure regulation involves renal
regulation of blood volume via the renin-angiotensin
mechanism and aldosterone mechanism.
• Increased blood osmolarity stimulates release of
antidiuretic hormone (ADH), which promotes
reabsorption of water, and excites the thirst center,
resulting in increased blood volume and blood pressure.