Micturition is the act of urination and includes both a storage phase and a voiding phase. Animals presenting with urinary
incontinence typically have one or more problems with the storage phase of micturition, which can usually be categorized as;
insufficient urethral closure pressure; failure of the bladder to relax and accommodate urine; or abnormal anatomy of the
bladder, ureter(s) and/or urethra.
The main organs involved in urination are the bladder and the urethra. The smooth muscle of the bladder, known as the detrusor
muscle, is innervated by sympathetic nerve fibers from the lumbar spinal cord and parasympathetic fibers from the sacral spinal
cord. The internal urethral sphincter consists of smooth muscle bundles that pass on either side of the urethra. More distal
along the urethra is the external urethral sphincter which is composed of skeletal muscle and is innervated by the somatic
pudendal nerve which originates in Onuf's nucleus in the cord.
In healthy animals, the lower urinary tract has two discrete phases: the storage phase and the voiding phase. The muscles
controlling micturition are controlled by both the autonomic and somatic nervous systems.
During the storage phase the internal urethral sphincter remains tense and the detrusor muscle relaxed by sympathetic stimulation.
The storage phase is controlled via stimulation of beta receptors in the bladder wall; causing detrusor muscle relaxation
and alpha-1 receptors in the proximal urethra; causing urethral contraction. Sympathetic (adrenergic) input from the hypogastric
nerve regulates the stimulation of these receptors. Skeletal muscle in the more distal urethra also contributes to urethral
closure pressure and continence. This skeletal muscle is under voluntary control and is innervated by the somatic nervous
system, principally through the pudendal nerve. Stimulation of the pudendal nerve with the neurotransmitters norepinephrine
(NE) and serotonin (5-HT) results in contraction of the striated component of the urethral sphincter.
During voiding, parasympathetic stimulation causes the detrusor muscle to contract and the internal urethral sphincter to
relax. As the bladder fills, sensory receptors in the bladder wall ascend the spinal cord to both the pontine micturition
center and the cerebrum transmit the need to urinate. Once the voluntary signal to begin voiding has been issued, neurons
in pontine micturition center fire maximally, causing excitation of sacral preganglionic neurons. The firing of these neurons
results in contraction of the detrusor muscle and expulsion of urine from the bladder. The pontine micturition center also
causes inhibition of Onuf's nucleus, resulting in relaxation of the external urinary sphincter. Under parasympathetic (cholinergic)
control via the pelvic nerve, alpha-adrenergic input to the bladder neck and proximal urethra is inhibited resulting in relaxation.
Mechanism of storage and voiding reflexes. A. Storage reflexes. B. Voiding reflexes. (From Chancellor MB, Yoshimura N: Physiology and pharmacology of the bladder and urethra. In Walsh PC (ed):
Campbell's Urology, pp 831–886. Philadelphia, Saunders, 2002).
Urethral sphincter mechanism incompetence
In canines, incontinence is most often a result of inadequate urethral closure pressure. Urethral sphincter mechanism incompetence
(USMI) is also known as "spay incontinence" or "hormone responsive incontinence". USMI is very common occurring in up to 30%
of spayed dogs; most frequently in young to middle-aged, larger-breed dogs that have been spayed in the past 4 years. Factors
contributing to the development of USMI may include an age related decline in collagenous support structures around the urethra
and/or a decrease in sensitivity of adrenergic receptors within the urethra. An abnormally positioned bladder, obesity and
anatomic abnormalities in the vagina and vestibule may also contribute to the problem. Although much more common in females,
USMI may occur in males as well.