SYMPATHETIC NERVOUS SYSTEM
The Sympathetic Nervous System
The sympathetic nervous system is even more automatic and
only exceptionally susceptible to any voluntary control.
When the environmental temperature is raised on a hot
summers day, the increased temperature initiates several
automatic responses. Thermal receptors convey stimuli to
sympathetic control centers of the brain from which
inhibitory messages travel along the sympathetic nerves to
the blood vessels of the skin resulting in dilatation of the
cutaneous blood vessels, thereby greatly increasing the flow
of blood to the surface of the body from where heat is lost
by radiation from the surface of the body. Dilatation of the
blood vessels in this way tends to lower the blood pressure
and to promote oozing or transudation of the fluid from the
capillaries which may result in swelling of the dependent
limbs. Thus, fine adjustments in sympathetic control of
vascular contraction and "tone" are required to prevent
excessive vascular dilatation and undue reduction in blood
pressure. Otherwise, this might result in severe
gravitational pooling of blood in the lower limbs thereby
reducing blood flow to the brain and causing fainting
spells, to which individuals with impaired sympathetic
nervous functions are very susceptible. The sympathetic
nervous system responds to environmental heat in another
important way. The rise in body temperature is sensed by the
hypothalamic center from which stimuli emanate via
sympathetic nerves to the sweat glands, resulting in
appropriate sweating. This serves to cool the body by the
loss of heat resulting from evaporation of the sweat, aided
by a cool breeze. The only really voluntary input that we
have to facilitate cooling in a warm environment is to get
into a pool, a cold shower, or an air-conditioned room! We
cannot voluntarily influence the dilatation of our blood
vessels or the adequacy of our sweating in response to heat
in other ways.
Control of the rate and strength of cardiac contractions is
also under the predominant control of the sympathetic
nervous system. Thus, a fall in blood pressure resulting
from traumatic injury causing blood loss is sensed by
pressure-sensitive parts of the arteries called
baroreceptors. Evidence of reduced arterial distension is
sensed by these baroreceptors and conveyed by the
parasympathetic (mainly the glossopharyngeal) nerves to the
cardiovascular control center in the medulla, called the
nucleus tractus solitarii. From these nuclei sympathetic
stimuli conveyed by the cardiac nerves cause acceleration of
the heart rate, probably complemented by simultaneous
reduction in the parasympathetic stimuli via the vagus
nerves which slow the heart rate. Although pain, anxiety,
fear and injuries or blood loss would involuntarily increase
the sympathetic stimulation to cardiac acceleration, most of
us are unable to influence either this effect or the
consequences of blood loss per se on cardiac acceleration.
