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MCB 32, FALL 2000
REGULATION OF ARTERIAL BLOOD PRESSURE
Reading: Chapters 8 and 9.
I.
Pressures and flows in the cardiovascular system
Systolic pressure is the highest pressure during any one beat of the heart, while
diastolic pressure is lowest pressure.
Pressure gradients within the CV system: Periodic high pressure in ventricles is
dissipated as blood circulates back to the veins and atria, which have only very low
pressure, nearly zero. Thus, the energy of contraction of the ventricles (expressed as a
pressure) has been nearly entirely dissipated as the blood has cirulated from the left
ventricle through the systemic circulation back to the right atrium. Similarly, though the
pressures in the pulmonary circulation are much lower than in the systemic circulation,
this pressure energy is nearly entirely dissipated as it circulates through the pulmonary
circulation back to the left atrium.
Note also oxygen conc. changes abruptly at systemic and lung capillaries, where
exchange of oxygen and carbon dioxide occurs.
Note high pressures in systemic arteries and arterioles and low pressures in veins.
Pulmonary circulation pressures in general are all lower than systemic circulation.
Smooth blood flow is silent (laminar).
Flow is proportional to the pressure gradient (e.g., between points one and two)
and inversely proportional to resistance of vessel between these two points:
F = (P1-P2)/R
Resistance to blood flow is determined primarily by the size of the vessel, which
is controlled by contraction and relaxation of blood vessel smooth muscle; larger vessel,
smaller resistance and vice versa. Resistance is inversely proportional to radius to 4th
power. See Figs 9.13 and 9.14.
Resistance to blood flow is larger in smaller vessels. The overall resistance of the
circulatory system is determined primarily by the resistance of the arterioles, even though
the capillaries are much smaller at the level of each individual vessel. The low resistance
of the capillaries is due to the fact that there are so many of them compared to the number
of arterioles. Thus, regulation of resistance to blood flow is controlled by controlling the
arteriolar resistance. People with abnormally high resistances in their arterioles often
have high blood pressure.
Since blood pressure averages about 100 mm Hg in the aorta and large arteries,
while it is about zero in the vena cava and right atrium, the above equation is often
substituted as follows:
blood flow = cardiac output = 5 liters/min
P1 = arterial pressure = 100 mm Hg
P2 = venous pressure = 0 mm Hg
R = peripheral resistance
and cardiac output = CO (5 liters/min) = (Part– Pven )/PR = Part/PR
Volume of blood is not distributed equally through the CV system: small
amounts in heart, arteries and capillaries, large amount in veins. Small amount in lung
blood vessels too.
II.
Control of blood flow at the local tissue level
Blood flow to individual tissues can be controlled by contraction or relaxation of
smooth muscles surrounding the arterioles and also around the entries to capillary beds,
the pre-capillary sphincters. These smooth muscles are controlled by factors released
from the tissues surrounding them. When the cells in the tissues alter their metabolic
activities, they release altered amounts of the metabolic factors, which diffuse over to the
smooth muscles to control their contraction and, thus, the flow of blood through the
vessels. For example, during exercise, muscle metabolism increases production of lactic
acid, CO2 and AMP (break down from ATP), and these diffuse from the cells to the
smooth muscles of the arterioles and precapillary sphincters, causing them to relax and
dilate, increasing blood flow through them. This automatically increases blood flow to a
metabolically active tissue. This is called exercise hyperemia. Another example occurs
during the increased blood flow following an ischemic episode (i.e., decreased blood
flow). This is called reactive hyperemia and is described in the textbook on page 253.
III.
Negative feedback regulation of blood pressure, example of homeostasis
Arterial blood pressure must be maintained at the proper level to insure blood
flows properly, but it cannot get too high or there is damage to the blood vessels, leading
to atherosclerosis, hardening of the arteries. Regulation occurs by negative feedback,
which refers to the situation in which a change in some controlled variable (e.g., decrease
in blood pressure) leads to a series of changes that results in the opposite change in the
controlled variable back to its control level. This maintenance of a steady state is called
homeostasis.
IV.
Mechanisms for controlling blood pressure Figs 9.18 and 9.19
All of the following are important for controlling arterial blood pressure:
Blood volume needs to be maintained. Normal value is 5 liters. This can be
decreased by about 1 liter without much effect (most of it comes from the veins, where
there is little effect on pressure), but loss of too much blood will lead to a drop in blood
pressure.
Arteriolar constriction and relaxation are also important. Increased constriction of
arterioles leads to increases in pressure due to increased peripheral resistance, while
decreased constriction leads to drops in pressure due to decreased peripheral resistance.
Heart rate and stroke volume, which in turn are regulated by autonomic nerves
and venous return, are also important. Increased heart rate and stroke volume lead to
increases in blood pressure.
V.
Pressure sensors: baroreceptors
The body has a variety of pressure receptors for sensing arterial and venous
pressures. All of them are pressure receptors that respond to changes in stretch of the
vessel they are located in by sending action potentials to the central nervous system.
More pressure, more stretch of the vessel, more action potentials sent to the CNS,
informing the system of the state of the arterial blood pressure. The most prominent and
important baroreceptors are located in the walls of the arch of the aorta and in the carotid
sinus; also in heart.
VI.
Control center: medulla oblongata
The baroreceptors send impulses to the medulla oblongata, which integrates the
information and then sends out the appropriate responses. When pressure has decreased,
sympathetic nerves are triggered, which then send out action potentials to the heart and
the blood vessels.
In the heart, sympathetic nerves release norepinephrine  increase rate of
depolarization  increase frequency of AP in SA node, which increases rate and strength
of contraction. Sympathetic nerves to the smooth muscles in the blood vessels causes
them to contract more strongly, leading to increased resistance, which elicits increases in
blood pressure to counteract the original decrease in pressure.
When pressure increases, parasympathetic nerves are triggered.
Parasympathetic nerves release acetylcholine  decrease rate of depolarization
 reduce frequency of AP in SA node, leading to reduction in cardiac output and
decrease in blood pressure. There is also a reduction in the sympathetic effects on the
blood vessels, which can cause them arteriolar smooth muscle to relax, also leading to
reductions in blood pressure.
VII.
Control of cardiac output
CO (liters/min) = stroke volume (ml/beat) x heart rate (beats/min)
Normal human CO = 5 l/min = 72 ml/beat x 70 beats/min
Control by changing heart rate (sympathetic increase, parasympathetic decrease)
and stroke volume.
Stroke volume is changed by altering contractility of heart muscle, usually
increased by sympathetic nerves. This increases amount of force generated by the
myosin and actin, often through changes in cell [Ca].
Stroke vol also changed by alterations of size of heart. with increases in venous
return leading to increases in contractility of the heart.
VII.
Integrated activity: hemorrhage Fig. 9.19