Human Physiology, An Integrated Approach

Eighth Edition

Chapter 15
Blood Flow and the
Control of Blood
Pressure
Figure 15.1 A functional model of the cardiovascular system
15.1 The Blood Vessels
• Walls of blood vessels contain smooth muscle, and elastic and fibrous
connective tissue
• Wall thickness varies in different vessels
• Inner layer is endothelium
– Secretes paracrine factors
▪ Regulates blood pressure, blood vessel growth, and absorption

• Blood vessels contain

vascular smooth muscle
– Arranged in circular or
spiral layers
– Vasoconstriction and
vasodilation
– Muscle tone is a state of
partial contraction
Arteries and Arterioles Carry Blood Away from the Heart
• Arteries
– Act as pressure reservoir
– Thick layers of vascular smooth
muscles
– Lots of elastic and fibrous connective
tissue

• Arterioles
– Site of variable resistance
▪ Control Blood Pressure!
– Part of the microcirculation
– Less elastic and more muscular

• Metarterioles
– Branches of arterioles
– Partial smooth muscle layer
– Precapillary sphincters open and
close to direct blood flow to
capillaries or venous circulation
Exchange Takes Place in the Capillaries
Capillaries
• Smallest vessels
• Primary site of exchange between
blood and interstitial fluid
• Walls (different than arterioles)
– Better exchange with tissue
▪ Lack smooth muscle
▪ Flat layer of endothelium
▪ Basal lamina

• Pericytes (form blood-brain barrier)

– Contractile cells associated with
capillaries
– Contribute to capillary
impermeability
– Secrete paracrine factors that
promote vascular growth and
differentiation
Blood Flow Converges in the Venules and Veins
• Venules
Valves ensure one-way flow in veins
– Receive blood from capillaries
– Thin exchange epithelium
– Little connective tissue
– Convergent pattern of flow

• Veins take blood back to the

heart
– Act as volume reservoir
▪ Hold >50% of bodies blood!
– Thin walls of vascular smooth
muscles
– Contain one-way valves,
prevent backward flow
– More numerous than arteries
– Lie closer to the body surface
– Less elastic tissue
Angiogenesis Creates New Blood Vessels
• Angiogenesis is development of new blood vessels
– Necessary for
▪ Normal development, Wound healing and uterine lining growth
– Enhances heart and skeletal muscle blood flow

• Controlled by cytokines (angiogenic and antiangiogenic)

– Promoted by vascular endothelial growth factor (VEGF) and fibroblast
growth factor (FGF)
– Inhibited by angiostatin and endostatin (from “stasis” = standing still)

• Regulating angiogenesis could prevent disease

– Inhibiting malignant tumor growth
– Promoting collateral circulation in coronary heart disease
15.2 Blood Pressure
• Blood pressure is highest in arteries and lowest in veins
– Pulse pressure measure of strength pressure wave produced by
ventricular contraction
▪
▪ Decreases over distance due to
friction
– Venous return aided by valves,
skeletal muscle pump, and
respiratory pump
Figure 15.5 Arteries are a pressure reservoir

By sustaining the driving pressure for blood flow

during ventricular relaxation, the arteries keep blood
flowing continuously through the blood vessels.
15.2 Blood Pressure
• Arterial blood pressure reflects the driving pressure for blood flow
– Mean Arterial Pressure (MAP) represents driving pressure
▪
– Hypotension is lower than normal MAP,
– Hypertension is higher than normal MAP
• Blood pressure is estimated by sphygmomanometry
– Korotkoff sounds
Cardiac Output and Peripheral Resistance Determine Mean Arterial Pressure
• MA P

• Blood flow into aorta = cardiac output (C.O) of left ventricle

• If flow in exceeds flow out of aorta then blood volume increases and MAP increases
• If flow out exceeds flow in of aorta then blood volume decreases and MAP decreases
• Changes in blood volume affect blood pressure
– Blood volume is relatively constant
▪ Some gain and loss throughout the day
▪ If blood volume increase, then pressure increases
– Kidney is responsible for removing excess fluid volume
▪ If blood volume decrease, then pressure decreases
– Lost fluid volume compensated through drinking or intravenous infusion
– Vasoconstriction and sympathetic stimulation of heart
Watch: Factors Affecting Blood Pressure
15.3 Resistance in the Arterioles
• Arteriolar resistance is influenced by both local and systemic control mechanisms
– Local control, sympathetic reflexes, hormones
• Myogenic autoregulation adjusts blood flow (local control)
– Vascular smooth muscle regulates its own state of contraction
– Stretched vascular smooth muscle mechanically-gated Ca2+ channels
▪ Contracts to resist stretching
• Paracrine signals influence vascular smooth muscle (including the gases O2, CO2, & NO)
– Secreted by vascular epithelium or nearby cells
▪ Active hyperemia (high metabolism, low O2) vs. reactive hyperemia (low blood flow)
▪ Vasodilator Nitric oxide (synthesized due to local hypoxia)
▪ Kinins and histamine (inflammation) are potent vasodilators
Table 15.2 Chemicals Mediating Vasoconstriction and
Vasodilation
Vasoconstriction
Chemical Physiological Role Source Type
Norepinephrine (α-receptors) Baroreceptor reflex Sympathetic neurons Neurotransmitter
Serotonin Platelet aggregation, smooth muscle Neurons, digestive tract, Paracrine signal,
contraction platelets neurotransmitter
Endothelin Local control of blood flow Vascular endothelium Paracrine
Vasopressin Increases blood pressure in hemorrhage Posterior pituitary Neurohormone
Angiotensin II Increases blood pressure Plasma hormone Hormone

Vasodilation
Chemical Physiological Role Source Type
Epinephrine (β2-receptors) Increase blood flow to skeletal muscle, heart, liver Adrenal medulla Neurohormone
Acetylcholine Erection reflex (indirectly through NO production) Parasympathetic neurons Neurotransmitter
Nitric oxide (NO) Local control of blood flow Endothelium Paracrine signal
Bradykinin (via NO) Increases blood flow Multiple tissues Paracrine signal
Adenosine Increases blood flow to match metabolism Hypoxic cells Paracrine signal
Increase blood flow to match metabolism Cell metabolism Paracrine molecule
Histamine Increases blood flow Mast cells Paracrine signal
Natriuretic peptides (example: Reduce blood pressure Atrial myocardium, brain Hormone, neurotransmitter
ANP)
Vasoactive intestinal peptide Digestive secretion, relax smooth muscle Neurons Neurotransmitter, neurohormone
The Sympathetic Branch Controls Most Vascular Smooth Muscle
Neural and hormonal signals
– Atrial natriuretic peptide (ANP)  Vasodilation
– Angiotensin II  Vasoconstriction
Sympathetic control
– Sympathetic innervation of most systemic arterioles
▪ Exception: vasculature of erectile tissue (penis and clitoris) Parasym.&NO
▪ Norepinephrine maintains arteriolar tone
– Binds α receptors → vasoconstriction
– Adrenal medulla releases epinephrine into blood
▪ Binds α receptors with very low affinity → vasoconstriction (Digestion)
▪ Binds β2 receptors on vascular smooth muscle of heart, liver, and skeletal
muscle arterioles → vasodilation (fight or flight)
Figure 15.11(b) Resistance and Flow
15.4 Distribution of Blood to the Tissues
• Blood distribution varies according to
metabolic need of individual tissues
• Governed by
– Local control mechanisms
– Homeostatic reflexes
• Possible because arterioles are arranged in
parallel
– Flow in aorta = Flow in all arterioles
– Individual arterioles regulate own flow,
compensated by remaining arterioles
• Cerebral blood flow stays nearly constant
• Coronary blood flows parallels the work
of the heart
▪ Low tissue oxygen → myocardial cells
release adenosine → dilation of
coronary arteries

During exercise skeletal muscle goes from 20% of C.O. to up to 85%

Blood flow through
individual blood
vessels is determined
by the vessel’s
resistance to flow

Arteriolar resistance in most

tissues of the body is a balance
between autonomic control by the
brain and local control by tissue
metabolites and paracrine signals.

However, two critical organs, the

brain and the heart, are so
dependent on a steady supply of
blood and oxygen that neural control
of their arterioles plays only a small
part in maintaining adequate
perfusion. In these two organs,
tissue metabolism is the primary
factor that determines arteriolar
resistance
15.5 Regulation of Cardiovascular Function
• Cardiovascular control center (CVCC) (also responds to body temp. & digestion)
• The baroreceptor reflex controls blood pressure
– Baroreceptors (mechanoreceptors) in carotid arteries and aorta
▪ Produce continuous (tonic) action potential to brainstem
▪ Changes in pressure reflected changes in frequency of action potential
– Always functioning

• Orthostatic hypotension triggers the baroreceptor reflex

– Orthostatic hypotension decrease in blood pressure due to postural change
▪ For example, laying to standing
– Failure to compensate may lead to decreased delivery of oxygen to brain
▪ Light-headedness or dizziness
Figure 15.14(b) Cardiovascular Control
Figure 15.15 Integration of resistance changes and cardiac output
Other Systems Influence Cardiovascular Function

• Arterial chemoreceptors activated by low O2  increased

cardiac output
• Adaptive integration between respiratory and cardiovascular
systems
• Blood pressure is modulated by hypothalamus and cerebral
cortex
– Learned and emotional responses
▪ Vasovagal syncope (fainting at the sight of blood)
• Blood pressure is closely tied to body fluid balance in the
kidney
stops
15.6 Exchange at the Capillaries
• Plasma and cells exchange materials across thin capillary walls
– Most cells are located within 1-3 cell widths (0.1 mm of the nearest capillary)
• Capillary density is related to metabolic activity of cells
• Capillaries have the thinnest walls
– Single layer of flattened endothelial cells
▪ Supported by basal lamina
• Continuous capillaries (leaky): muscle, connective and neural tissue
• fenestrated capillaries (kidney and intestine):
• Sinusoids
– Modified capillary vesselto allow blood cells and protein to cross endothelium
– Bone marrow, liver, and spleen
Velocity of Blood Flow Is Lowest in the Capillaries
• Velocity of flow important for material exchange efficiency (think drive-through)
• At constant flow rate, velocity of flow is higher in smaller diameter tubes
• Primary determinant of velocity is total cross-sectional area of all capillaries
– Fastest flow in artery system
– Slowest flow in capillaries and venules
Most Capillary Exchange Takes Place by Diffusion and Transcytosis
• Exchange between plasma and interstitial fluid (outside cells) occurs by
– paracellular pathway (movement between cells)
– endothelial transport (movement through cells)

• Movement by diffusion
– Small dissolved solutes and gases
– Depending on lipid solubility and concentration gradient

• Vesicular (by a vesicle) transport

– Larger solutes and proteins
– In most capillaries, large molecules (including selected proteins) are
transported by transcytosis
Capillary Filtration and Absorption Takes Place by Bulk Flow
• Bulk flow is mass movement as a result of hydrostatic or osmotic
pressure gradients
• Filtration: fluid movement out of capillaries
– Caused by hydrostatic pressure (PH); IF hydrostatic pressure (PIF) is
negligible
▪ PH decreases over length of capillary due to friction

• Absorption: fluid movement into capillaries

– Caused by colloid osmotic pressure (π), also called oncotic pressure
▪ Due to presence of proteins in capillaries (have plasma proteins)
(πcap = 25 mm Hg), IF has none (πIF = 0 mm Hg.

• Net pressure determines direction of bulk flow;

– Net filtration at arterial end
– Net absorption at venous end
Figure 15.18 Capillary fluid exchange
15.7 Lymphatic System
1. Returns fluid and proteins to
circulatory system
2. Picks up fats absorbed in G.I. tract
and transferring it to circulatory system
3. Serves as filter for pathogens
• Allows for one-way movement of
interstitial fluid into the circulatory
system
– Lymph
– Lymph capillaries are blind-ended
– Lymph vessels with semilunar valves
empty into venous circulation
– Lymph nodes

• Edema is accumulation of fluid in the

interstitial space
– Inadequate drainage of lymph or
filtration greater than absorption
15.8 Cardiovascular Disease
• Risk factors for CVD include smoking and obesity

• Not controllable: sex, age, family history

• Controllable: smoking, obesity, sedentary lifestyle, untreated hypertension
• Some genetic factors can be modified by lifestyle
– Diabetes mellitus: metabolic disorder that contributes to development of
atherosclerosis
• Coronary heart disease (CHD) accounts for the majority of cardiovascular
disease deaths and is the single largest killer of Americans

• Atherosclerosis is an inflammatory process

– Increased blood cholesterol and triglycerides
– High-density lipoprotein-cholesterol (HDL-C) is “healthy” cholesterol
– Low-density lipoprotein-cholesterol (LDL-C) is “lethal” cholesterol
▪ apoB combines with LDL receptors on cells  drop off
cholesterol in cells (NECESSARY FOR CELLS)
 The
development of
atherosclerotic
plaques

Atherosclerosis is now
considered to be an
inflammatory process in which
macrophages release enzymes
that convert stable plaques to
vulnerable plaques

8. Stable plaques have thick

fibrous caps that separate the
lipid core from the blood and do
not activate platelets.

Vulnerable plaques have thin

fibrous caps that are more likely
to rupture, exposing collagen
and activating platelets that
initiate a blood clot (thrombus)
9.
Hypertension Represents a Failure of Homeostasis
• The risk of developing cardiovascular disease doubles with each mm
Hg increase in blood pressure over a baseline value of
• Primary (or essential) hypertension
(90%)
– Has no clear cause other than
hereditary (lifestyle control)
– Cardiac output is usually normal, but
increased peripheral resistance
• Secondary hypertension (10%)
– Due to an underlying pathology
• Risk factor for atherosclerosis
• Heart muscle hypertrophies then
– pulmonary edema and congestive
heart failure
• Treatment: calcium channel blockers,
diuretics, beta-blocking drugs, and
Angiotensin Blockers (ACE inhibitors, and
angiotensin receptor blockers)