Give
an account of the regulation of arterial blood pressure in man.
Outline:
·
Short and long term
regulation
·
Neural control through
vasomotor center:
- afferent: baroreceptors
- heart: vagal control
- blood vessels: sympathetic control
·
Long-term control by
kidneys: renin-angiotensin-aldosterone axis
Essay:
The normal arterial blood pressure in man is between 90 and 100 mmHg. Too
low a blood pressure decreases tissue perfusion while too high a pressure
imposes excessive work load upon the heart. Therefore it is essential to
regulate blood pressure within narrow limits, minimizing any major fluctuations
in it. There are two systems of regulation: a short term system mediated by the
autonomic nervous system which buffers any changes in blood pressure in daily
life (due to exercise, changing of position of body, etc.); and a long term
system of control by the kidneys which returns a previously hypotensive or
hypertensive state back to normal (renal compensation in cardiac failure, etc).
The autonomic nervous system exerts its control over regulation of
arterial pressure through the sympathetic and parasympathetic fibers and reflex
mechanisms of the baroreceptors and to a lesser extent, the chemoreceptors. The
activities of the autonomic nervous system and reflex receptors are under direct
control of the vasomotor center which may be regulated by the higher brain
centers.
The vasomotor center can be divided functionally into a vasoconstrictor,
vasodilator and sensory area. The vasoconstrictor area is located in the
anterolateral portions of the upper medulla. The neurons in this area are known
as the C1 group of cells. Their fibers are distributed throughout the spinal
cord, where they excite the vasoconstrictor neurons of the sympathetic nervous
system.
The vasodilator area is located in the anterolateral portions of the
lower half of the medulla. The neurons in this area are known as the A1 group of
cells. Their fibers project upward to the vasoconstrictor area and mediate
inhibition of vasomotor discharge, thus causing vasodilation.
The sensory area contains the A2 groups of cells. It is located in the
tractus solitarius in the posterolateral portion of the medulla and lower pons.
The neurons of this area receive afferent nerve signals from the vagus and
glossopharyngeal nerves. The output signals from this sensory area then helps to
control the activities of both the vasoconstrictor and vasodilator areas, thus
providing reflex control of many circulatory functions.
Under normal conditions, the vasoconstrictor area of the vasomotor center
transmits signals continuously to the sympathetic nerves over the entire body.
These impulses maintain a partial state of contraction in the blood vessels
called vasomotor tone which plays an important role in maintaining the blood
pressure and cardiac output. The medial portion of the vasomotor center transmit
impulses continuously through the vagus nerve to the heart to decrease heart
rate (vagal tone).
The baroreceptors are stretch receptors in the walls of the heart and
blood vessels. The carotid sinus and aortic arch receptors monitor the arterial
circulation. Receptors are also located in the walls of the right and left
atria, the pulmonary veins, in the wall of the left ventricle, and in the
pulmonary circulation. These receptors are known collectively as the
cardiopulmonary receptors. The baroreceptors are stimulated by distention of the
structures in which they are located, and so they discharge at an increased rate
whenthe pressure in these structures rises. When blood pressure drops, due to
postural change from supine to standing position, the stretch of the arterial
wall decrease. This is sensed by the baroreceptors which decrease their
inhibitory discharge to the vasoconstrictor area of the vasomotor center. The
resultant increase in sympathetic discharge raises blood pressure back to
normal.
Baroreceptors are responsive to mean pressures between 50-170 mmHg. The
primary purpose of the arterial baroreceptor system is to reduce the daily
variation in arterial pressure. The baroreceptors reset themselves to the
prevailing pressure after 1-2 days. Therefore, they function primarily to
stabilize acute variations in blood pressure from a day to day basis but are
ineffective for long term regulation of blood pressure. The chemoreceptors are
located in the carotid and aortic bodies. Strictly speaking, they are not
directly involved in the regulation of arterial blood pressure as they respond
primarily to levels of carbon dioxide, oxygen and hydrogen ions concentration in
the blood rather than a change in blood pressure. Their predominant role is the
control of respiration. They are stimulated only when arterial pressure falls
below 80 mmHg.
The kidneys is the chief regulator of long term blood pressure by
regulating blood volume in response to its changes. The smooth muscle cells in
the afferent and efferent arterioles are the site of synthesis, storage and
release of renin. A decrease in effective circulating blood volume and perfusion
pressure activates the sympathetic nerve fibers innervating the afferent and
efferent arterioles as well as the afferent arteriole itself, which acts as a
high-pressure baroreceptor, detecting any changes in the perfusion pressure to
the kidneys. The end result is an increase in renin secretion. Renin functions
solely as a proteolytic enzyme, cleaving angiotensinogen, which is produced by
the liver, to yield a 10-amino acid peptide, angiotensin I. Angiotensin I is
further cleaved to an 8-amino acid peptide, angiotensin II, by a converting
enzyme found on the surface of vascular endothelial cells. Angiotensin II
stimulates aldosterone secretion by the adrenal cortex, and arteriolar
vasoconstriction, which increases blood pressure. It enhances NaCI reabsorption
by the proximal tubule and stimulates ADH secretion and thirst. All these
results in the conservation of sodium, and replenishment of water to raise the
ECF volume and therefore the blood pressure back to normal. The kidneys play an
important role in the restoration of cardiac output in the aftermath of cardiac
failure.