260 Chapter 9
parasympathetic division on the internal urethral sphincter. This
smooth muscle, together with the external urethral sphincter (com-
posed of skeletal muscle), guards the exit of the bladder to the ure-
thra. When parasympathetic nerve activity to the detrusor muscle
of the bladder increases to stimulate bladder contraction, sympa-
thetic activity to the internal sphincter muscle must decrease to
allow the sphincter to relax and the bladder to empty. Voluntary
control of micturition is discussed in chapter 17, section 17.1.
Organs Without Dual Innervation
Although most organs receive dual innervation, some receive
only sympathetic innervation. These include:
- the adrenal medulla;
- the arrector pili muscles in the skin;
- the sweat glands in the skin; and
- most blood vessels.
In these cases, regulation is achieved by increases or
decreases in the tone (firing rate) of the sympathetic fibers. Con-
striction of cutaneous blood vessels, for example, is produced by
increased sympathetic activity that stimulates alpha- adrenergic
receptors, and vasodilation results from decreased sympathetic
nerve stimulation.
The sympathoadrenal system is required for nonshiver-
ing thermogenesis: animals deprived of their sympathetic
system and adrenals cannot tolerate cold stress. The sympa-
thetic system itself is required for proper thermoregulatory
responses to heat. In a hot room, for example, decreased
sympathetic stimulation produces dilation of the blood ves-
sels in the skin, which increases cutaneous blood flow and
provides better heat radiation. During exercise, by contrast,
sympathetic activity increases, causing constriction of the
blood vessels in the skin of the limbs and stimulation of
sweat glands in the trunk.
The sweat glands in the trunk secrete a watery fluid in
response to cholinergic sympathetic stimulation. Evaporation
of this dilute sweat helps to cool the body. The sweat glands
also secrete a chemical called bradykinin in response to sym-
pathetic stimulation. Bradykinin stimulates dilation of the
surface blood vessels near the sweat glands, helping to radi-
ate some heat despite the fact that other cutaneous blood ves-
sels are constricted. At the conclusion of exercise, sympathetic
stimulation is reduced, causing cutaneous blood vessels to
dilate. This increases blood flow to the skin, which helps to
eliminate metabolic heat. Notice that all of these thermoregula-
tory responses are achieved without the direct involvement of
the parasympathetic system.Control of the Autonomic Nervous
System by Higher Brain Centers
Visceral functions are largely regulated by autonomic reflexes.
In most autonomic reflexes, sensory input is transmitted to brain
centers that integrate this information and respond by modify-
ing the activity of preganglionic autonomic neurons. The neural
centers that directly control the activity of autonomic nerves are
influenced by higher brain areas, as well as by sensory input.
The medulla oblongata of the brain stem controls many activ-
ities of the autonomic system. Almost all autonomic responses
can be elicited by experimental stimulation of the medulla, where
centers for the control of the cardiovascular, pulmonary, urinary,
reproductive, and digestive systems are located. Much of the
sensory input to these centers travels in the afferent fibers of the
vagus nerve—a mixed nerve containing both sensory and motor
fibers. The reflexes that result are listed in table 9.8.
Although it directly regulates the activity of autonomic
motor fibers, the medulla itself is responsive to regulation by
higher brain areas. One of these areas is the hypothalamus, the
brain region that contains centers for the control of body tem-
perature, hunger, and thirst; for regulation of the pituitary gland;
and (together with the limbic system and cerebral cortex) for
various emotional states. Because several of these functions
involve appropriate activation of sympathetic and parasympa-
thetic nerves, many scientists consider the hypothalamus to be
the major regulatory center of the autonomic system.CLINICAL APPLICATION
Autonomic dysreflexia is a serious condition that can cause
stroke, pulmonary edema, and myocardial infarction (heart
attack) in people with spinal cord injuries at or above the
sixth thoracic level (T6) of the spinal cord. Spinal shock may
occur immediately after a spinal cord injury, especially if the
cord is completely transected. At first there is a loss of spi-
nal reflexes below the level of the injury, but after some time
the reflexes reappear in an exaggerated state. In this con-
dition, a noxious sensory stimulus—usually from the urinary
bladder or colon—can evoke a strong response from the
sympathoadrenal system. Sympathetic nerves cause vaso-
constriction and increased heart rate, which raise the blood
pressure. Pressure receptors in arteries sense this, and send
signals via cranial nerves IX and X to the brain (chapter 14;
see fig. 14.27). In response, the brain directs an inhibition
of sympathetic activity and an increase in parasympathetic
activity, which normally maintain homeostasis. However, if
the person has a spinal cord injury at or above T6, the inhi-
bition of the sympathetic (thoracolumbar) response cannot
descend below the injury. High sympathetic nerve activity is
maintained below the level of the injury, producing vasocon-
striction that can cause dangerous hypertension as well as a
cold skin and goose bumps. By contrast, sympathetic nerve
activity is decreased above the level of the injury, accompa-
nied by increased parasympathetic nerve effects. This results
in bradycardia (a slow heart rate), nasal congestion, and a
flushed, sweaty skin above the level of the spinal cord injury.
The bradycardia is insufficient to lower the dangerously ele-
vated blood pressure, and so autonomic dysreflexia requires
efforts to eliminate the noxious stimulus that provoked it, as
well as other measures.