Chapter 18: The Cardiovascular system: Blood Vessels
Objectives:
1. Describe the three layers that typically form the wall of a blood vessel, and state the function of
each.
2. Define vasoconstriction and vasodilation.
3. Compare and contrast the structure and function of the three types of arteries.
4. Describe the structure and functions of veins, and explain how veins differ from arteries.
5. Describe the structure and function of a capillary bed.
6. Define blood flow, blood pressure, and resistance, and explain the relationship between these
factors.
7. List and explain the factors that influence blood pressure, and describe how blood pressure is
regulated.
8. Define hypertension. Describe both its symptoms and consequences.
9. Explain how blood flow is regulated in the body in general and in its specific organs.
10. Outline the factors involved in capillary dynamics, and explain the significance of each.
11. Define circulatory shock. List several possible causes.
12. Provide examples of changes that often occur in blood vessels as a person ages.
Layers of blood vessels See figure 18.1
1. Lumen: the empty space inside the blood vessel
2. Tunica interna: innermost layer of endothelium, made of simple squamous epithelium (slick)
3. Tunica media: middle layer of circular smooth muscle and sheets of elastin. Innervated by
vasomotor nerve fibers of sympathetic division of ANS.
4. Tunica externa (adventitia): collagen fibers with nerve fibers, lymph vessels, some elastin, and
blood vessels.
Vasoconstriction: contraction of smooth muscle to decrease diameter of lumen
Vasodilation: relaxation of smooth muscle layer to increase diameter of lumen
Types of Blood Vessels: See Table 18.1, figure 18.2
Arteries: carry blood away from heart
1. Elastic: thick walled near heart (aorta & branches). Largest in diameter and most elastic.
Large lumen gives low-resistance (conducting arteries). If arteriosclerotic (hard), they may balloon out
into aneurysms.
2. Muscular or distributing: deliver blood to specific body organs. Have thickest tunica media
layer, active in vasoconstriction.
3. Arterioles: smallest artery, narrow down to single layer of smooth muscle. Controls blood
flow into capillaries through
response to neural and chemical influence. Constriction of
arterioles bypasses tissues served, dilation floods tissues served.
Capillaries: smallest vessels w/ just thin tunica interna. Just large enough for RBC’s to slip
through single file. Designed for exchange of materials (gases, nutrients, wastes) between blood and
interstitial fluid. See figure 18.3
1. Continuous: most common, found in skin and muscles, uninterrupted lining
2. Fenestrated: have pores covered by a membrane, for active absorption or filtration
(small intestine, kidneys)
3. Sinusoid: leaky capillaries to allow large molecules and blood cells to pass, as in liver,
bone marrow, lymphoid tissue and some endocrine glands. Blood flows sluggishly to provide time for
modification (nutrients into liver, bacteria destroyed and removed)
4. Capillary beds: interweaving networks with shunts. See figure 18.4
Venules: post capillary venules are extremely porous for fluid and WBC’s to leave blood stream
(as in inflammation). Large venules have thin tunica media and externa.
Veins: walls are thinner and lumen larger, but they do possess all three tunics as in arteries.
Tunica media contains little smooth muscle
and externa is thickest. 65% of blood in body is found
in veins at any one time (blood reservoir). Venous valves prevent backflow of blood and are formed from
folds of tunica interna (similar to semilunar valves). Most valves in veins of limbs.
1.Varicose: tortuous (twisty) and dilated due to incompetent valves; gravity and pressure
affect them. Varicose veins in anus are
hemorrhoids.
2. Anastomoses: connect vein to vein, artery to artery or artery to vein
Physiology of Circulation
1. Blood flow: actual volume flowing through a vessel, organ, or circulation in time (ml/min) = Cardiac
output.
2. Blood pressure: force/unit area exerted on wall of blood vessel (mmHg). Systemic arterial pressure
greatest in largest arteries near heart. The differences in blood pressure keep blood moving.
3. Resistance: opposition to flow, measure of amount of friction; peripheral resistance (PR)
a. Blood viscosity: internal resistance to flow due to thickness or stickiness of fluid.  viscosity,
 resistance,  blood pressure
b. Total blood vessel length: the longer the length of vessel, the greater the resistance, (an
extra lb or 2 of fat requires miles of
small vessels to serve it)
c. Blood vessel diameter: fluid close to the wall is slowed by friction. The blood in the center
flows freely. Resistance = 1/r4
Systemic blood pressure: greatest pressure near pump, this generates blood flow and pressure
results when flow is opposed by resistance.
See figure 18.5
Arterial blood pressure: 1. How much elastic arteries close to heart can be stretched (compliance or
distensibility) 2. Volume of blood forced into arteries at any time. It is pulsatile.
Systolic pressure = 120 mmHg, Diastolic pressure = 70-80 mmHg. The difference is pulse pressure.
Mean arterial pressure (MAP): it is the pressure that propels the blood to the tissues throughout the
cardiac cycle.
MAP = diastolic pressure + pulse pressure (sys-dia)
3
120/80 pressure = 93 mmHg MAP
Capillary blood pressure: 40 mmHg by the time it reaches the capillaries and 20 mmHg by the time it
leaves but 1. capillaries are fragile and 2. permeable and force filtrate or nutrients out of blood to
interstitial space.
Venous blood pressure: steady and changes little. No measurable BP in vena cava.
Venous return See figure 18.6
1. Respiratory pump: pressure changes in ventral body cavity during breathing pushes blood up
toward heart.
2. Muscular pump: skeletal muscle activity, along w/ valves keep venous blood moving in one direction
toward heart.
Maintaining blood pressure: BP = CO x PR (and blood volume) See figure 18.7
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Main factors affecting CO = venous return (for stroke volume) and neural/hormonal control (for
HR).
Parasympathetic cardioinhibitory center (through vagus nerve) is in charge of the resting heart
rate. During this time, SV is controlled by EDV (by venous return).
During stress, heart rate increases, SV increases due to contractility (and therefore,  ESV) and
therefore  CO and  MAP
Short-term neural controls of peripheral resistance
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
Alter blood distribution to tissues in response to demands (ex. shunt blood away from GI tract
during sympathetic stimulation)
Maintain MAP by altering blood vessel diameter (through vasoconstriction and vasodilation)
Vasomotor center: found in medulla oblongata w/ cardiac center; integrates blood pressure control by
altering CO and blood vessel diameter.
1. Baroreceptors: pressure receptors in carotid sinuses (to protect brain) and aorta (to keep up BP in
systemic circ.) send signals to vasomotor center when BP rises and stretches the receptors. This inhibits
the center in the medulla, resulting in vasodilation. A signal is also sent to stimulate parasympathetic
division to slow heart rate. See figure 18.8
A drop in MAP initiates vasomotor reflex to increase HR and CO.
2. Chemoreceptor initiated reflexes: (carotid and aortic bodies) a drop in O2 or pH in aortic arch
causes an increase in cardiac output and vasoconstriction.
Short-term chemical controls See Table 18.2: O2 and CO2 act on chemoreceptors but other
chemicals act directly on smooth muscle or vasomotor center. See figure 18.14
1. Adrenal medulla hormones: NE is vasoconstrictive. Epinephrine raises cardiac output by
increasing permeability to calcium.
2. Atrial natriuretic peptide: acts on blood volume and kidneys to lower BP. Antagonistic to
aldosterone, the kidneys will be stimulated to excrete Na + (and water follows salt) to lower blood volume
and also causes generalized vasodilation.
3. ADH: in response to dropping BP, this causes intense vasoconstriction during hemorrhage and water
retention by kidneys.
4. Angiotensin II: causes vasoconstriction in response to low BP.
5. Endothelium derived factors: endothelin is a potent vasoconstrictor that allows calcium entry into
smooth muscle, in response to low BP.
6. Nitric oxide: causes vasodilation, released from endothelium of blood vessels during high BP. Shortlived, but helps return BP to normal after sympathetic stimulation.
7. Inflammatory chemicals: histamine causes vasodilation
8. Alcohol: lowers BP by inhibiting ADH, depresses vasomotor center and is a vasodilator in skin
Long-term mechanisms and renal regulation See figure 18.9: a rising blood volume causing a
rise in BP stimulates kidneys to elimination water, which reduces blood volume and blood pressure. A
drop in blood volume causes kidneys to retain water and raise blood volume and pressure. See figure
18.10
1. Direct renal mechanism: when there is a rise in blood volume or pressure, the kidneys filter
faster, which decreases the time for reabsorpion of filtrate (namely water) and more fluid leaves as urine.
A drop in blood volume or pressure means water is conserved and returned to the blood stream during
slower filtration.
2. Indirect renal mechanism: renin-angiotensin mechanism from low BP is activated.
Juxtaglomerular cells of the kidney release rennin into blood that triggers production of angiotensin II. It
is a potent vasoconstrictor that increases rate of blood delivery to kidneys. It also stimulates release of
aldosterone from adrenal cortex and release of ADH. This then causes an increase in blood pressure.
Chronic hypertension: can be caused by diet, obesity, age, race, heredity, stress, smoking. Ways to
treat: diuretics, betablockers, calcium channel blockers, block epinephrine receptors, ACE inhibitors
(angiotensin converting enzyme)
Capillary dynamics See figure 18.13
Vasomotion: slow and intermittent flow of blood through capillaries
Diffusion: O2 and CO2, most nutrients and metabolic wastes pass between blood and interstitial
fluid by diffusion. See figure 18.15
Hydrostatic pressure (HP): force exerted by a fluid pressing against a wall. HP is the same as
capillary blood pressure (HPC). It tends to force fluids through capillary walls. HPC is higher at the
arterial end than the venous end. BP is opposed by HPIF acting outside the capillaries, pushing fluid
in. The net HP is the difference of HPC and HPIF .
Colloid osmotic pressure: created by presence in a fluid of large, nondiffusible molecules
(plasma proteins, namely albumin) that are prevented from moving through the capillary
membrane. These molecules draw water toward them whenever water concentration in their
vicinity is relatively lowerthan on the opposite side of the capillary membrane (ie. In the tissues).
OPC pulls water back into capillary blood.
Hydrostatic-Osmotic pressure interactions See figure 18.16
Net filtration pressure (NFP): fluid out at arterial end, osmotic forces dominate at
venous end. Net loss (more out than in) = 1.5 ml/min, returned to circulation by
lymphatics.
Circulatory shock: blood vessels are inadequately filled
Hypovolemic shock: large scale blood or fluid loss (hemorrhaging, vomiting, dehydration,
diarrhea, burns) See figure 18.17
 a rise in heart rate to compensate results in a weak, thready pulse
 an increase in vasoconstriction occurs to enhance venous return
 a sharp drop in BP is a late, but serious, sign
Vascular shock: blood volume is normal and constant. Poor circulation due to extreme
vasodilation (expansion of vascular bed). PR drops, followed by a rapidly dropping BP. Anaphylaxis,
septicemia (bacterial toxins are vasodilators), failure of sympathetic NS, even sunbathing can
cause this.
Anaphylaxis: loss of vasomotor tone due to an allergic reaction or other cause of the release of
histamine (a potent vasodilator)
Cardiogenic shock: pump failure, due to multiple myocardial infarcts
Atherosclerosis: aorta and coronary arteries most affected. Damage to endothelium triggers repair
processes that can go haywire, especially if many LDL’s (with cholesterol) are present. These LDL’s
deliver cholesterol to tissues which further complicates repair and proliferation of tunica interna and media
work to decrease the diameter of the lumen. Thrombi can develop and block even more.
Treatment/prevention: lower cholesterol and LDL, raise HDL. Reduce inflammation, coronary bypass
surgery, balloon angioplasty, change lifestyle.