Innervation Of Urinary System
The urinary system
receives a rich nerve supply from the autonomic nervous system, which is
accompanied by visceral afferent nerve fibers. The autonomic nervous system
facilitates bladder filling and stimulates emptying, whereas visceral afferent
fibers from the bladder convey sensations produced by distention.
Once toilet training is complete, voiding can be consciously inhibited by
somatic efferent fibers that stimulate contraction of the external urethral
sphincter. Likewise voiding can be consciously enhanced by contraction of the
diaphragm and abdominal wall muscles, which further compress the contracting
bladder.
Sympathetic
Anatomy. Sympathetic innervation of the urinary system
begins in the lower thoracic and upper lumbar (T10-L2 or 3) spinal cord
segments, where neurons of the intermediolateral (IML) cell column give rise to
presynaptic (preganglionic) sympathetic fibers. These fibers exit the CNS via the
anterior roots of the corresponding spinal nerves, traverse the initial parts
of those spinal nerves, then exit via white rami communicans to reach the
sympathetic trunks.
Within the sympathetic trunks, some fibers descend through the
paravertebral ganglia to lower levels, but all of them leave the trunks,
without synapsing, in visceral branches. These branches, also known as the
abdominopelvic splanchnic nerves, extend from the medial aspects of the trunks.
They include the lesser thoracic
(T10-11), least thoracic (T12), lumbar, and possibly
sacral splanchnic nerves. Together, these nerves convey presynaptic fibers to
the prevertebral ganglia, such as the celiac and aorticorenal ganglia, located
near the major branches of the abdominal aorta. The presynaptic neurons synapse
in these ganglia with postsynaptic neurons.
The pathway of sympathetic innervation to the kidneys and upper ureter
(see Plate 1-15) begins in presynaptic fibers originating in the T10-L1 levels
of the IML. These fibers travel through splanchnic nerves to synapse with
neurons of the superior mesenteric ganglion, aorticorenal ganglia, and the
small ganglia in the periarterial renal plexuses. Postsynaptic fibers reach the
kidney and upper ureter via periarterial plexuses and branches.
The pathway of sympathetic innervation to the remainder of the ureters
and urinary bladder begins with presynaptic fibers originating in the T12-L2(3)
levels of the IML. These fibers travel through lumbar (and possibly sacral)
splanchnic nerves and then the intermesenteric (aortic) plexus, then synapse
with neurons in the inferior mesenteric ganglion or small ganglia of the
aortic/hypogastric plexuses. Postsynaptic fibers descend into the pelvis via
aortic, hypogastric, and pelvic (vesical) plexuses to reach the ureters and
bladder.
Function. In the kidney, sympathetic tone has numerous
effects on both the vasculature and renal tubules. Adrenergic receptors are
located throughout the renal cortex and outer stripe of the outer zone of the
renal medulla, with the greatest density in the
juxtamedullary region of the inner cortex. Graded increases in renal
sympathetic tone cause renin release from juxtaglo merular granular cells (see
Plate 3-18), increase renal tubular sodium reabsorption, and decrease renal
blood flow (by constricting afferent arterioles). These combined effects can
contribute to the development and maintenance of hypertension. In experimental
animals, for example, renal denervation is known to prevent or ameliorate
hypertension. Likewise, in patients with drug-resistant essential hypertension,
catheter-based radiofrequency renal denervation results in substantial and
sustained reductions in systemic blood pressure.
Some renal sympathetic nerve fibers release dopamine, but there is no
evidence that dopamine released during sympathetic stimulation affects renal
function. Thus dopamine is not considered an endogenous neurotransmitter in the
kidney. Likewise, despite the presence of acetylcholinesterase, renal
sympathetic nerve stimulation is not affected by anticholinergic agents.
In the ureter, peristalsis is primarily myogenic in nature, driven by
specialized pacemaker cells (see Plate 1-27). The efferent and afferent fibers
of the extrinsic plexus, however, do appear to be involved in regulating the
pacemaker cells.
In the bladder, activation of adrenergic receptors causes relaxation of
the detrusor muscle, which facilitates bladder expansion during filling.
Meanwhile, activation of b adrenoceptors facilitates contraction of
the trigone muscle. In males, trigonal muscle is circularly arranged to form an internal urethral
sphincter, which prevents ejaculation into the bladder. As a result, stress may
interfere with the ability to urinate by contracting this muscle. In females,
in contrast, sphincteric arrangement of trigonal muscle is not evident.
Parasympathetic
Anatomy. Parasympathetic innervation of the urinary system
is derived from cranial and sacral sources. Both sources send presynaptic fibers all the way to the target organ,
where they synapse with intrinsic (intramural) postsynaptic neurons.
The cranial source, which innervates the kidneys and upper ureters, is
the vagus nerve; it conveys presynaptic fibers through the celiac and
aorticorenal ganglia to the intrinsic renal and upper ureteric plexuses.
The sacral source, which innervates the remainder of the ureters and
bladder, begins in the S2-S4 spinal cord segments, which contains neurons that
give rise to presynaptic parasympathetic fibers. These
fibers enter the initial portions of spinal nerves S2-S4 and then exit via
pelvic splanchnic nerves, which convey them to the intrinsic plexuses of the
ureters and bladder. Of note, the upper ureter may receive branches of these
parasympathetic fibers, even though its primary source of parasympathetic
innervation is the vagus nerve.
Function. In the kidney, the role of vagal (cholinergic)
function is unclear. In the ureter, parasympathetic stimulation probably
modulates intrinsic pacemaker cells.
In the bladder, parasympathetic stimulation triggers contraction of the
detrusor muscle and, by inhibiting sympathetic tone, also indirectly relaxes
the trigonal muscle. In males, relaxation of the trigonal muscle includes
relaxation of the internal urethral sphincter. The combination of detrusor
contraction and sphincter relaxation enables micturition.
Afferent
Afferent innervation from the urinary system carries pain sensations and
also plays a critical role in intrinsic reflexes. The pathways for pain
sensation depend on whether the organ is invested with serosa. In those organs
with serosa, such as the kidneys, abdominal ureters, and superior surface of
the bladder, afferent pain fibers follow the pathways of sympathetic innervation
in a retrograde direction until they reach spinal sensory ganglia. Referred
pain from these organs is experienced at the dermatomes corresponding to the levels where the presynaptic fibers
enter the sympathetic chain. The pain
of pyelonephritis, or of an impacted stone in the renal pelvis or abdominal
ureter, is experienced at levels T10-L1. The sensation of a distended bladder
is experienced in T12-L2.
In contrast, afferent fibers conveying pain from organs without serosa
(i.e., subperitoneal viscera, such as the neck of the bladder, terminal
ureters, prostate, cervix, and upper vagina), as well as fibers involved in
reflex arcs, generally follow the pathways of parasympathetic innervation in a
retrograde direction until they reach
cranial and sacral sensory ganglia. Thus, the visceral afferents conducting
pain impulses from subperitoneal viscera have cell bodies located in the S2-S4
spinal sensory ganglia, with sensations perceived in the corresponding
dermatomes. Mechanoreceptors and chemoreceptors that play a role in renorenal
reflexes also send projections along vagal afferent fibers to vagal sensory
ganglia. Likewise, the reflexive emptying of a moderately distended bladde ,
such as occurs in infants, is
transacted at sacral levels.