Publication: Innervation of the proximal urethra of ovariectomized and estrogen-treated female rats
Authors
Smith, P.G. ; Bradshaw, S.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The proximal urethra plays a central role in
maintaining urinary continence, and sympathetic
excitatory innervation to urethral smooth muscle is a
major factor in promoting tonic contraction of this organ.
Elevated estrogen levels are often associated with
incontinence in humans. Because elevated estrogen
levels result in degeneration of sympathetic nerves from
the closely related uterine smooth muscle, we examined
the effects of chronic estrogen administration on
proximal urethral innervation. Ovariectomized virgin
female rats received either vehicle or 17 ß-estradiol for 1
week, and smooth muscle size and parasympathetic,
sensory and sympathetic nerve densities were assessed
quantitatively throughout the first 3 mm of the proximal
urethral smooth muscle. In vehicle-infused
ovariectomized rats, parasympathetic nerves
immunoreactive for vesicular acetylcholine transporter
were most abundant, while calcitonin gene-related
peptide-immunoreactive sensory nerves and tyrosine
hydroxylase-immunoreactive sympathetic nerves were
less numerous. The densities of parasympathetic and
sensory nerves remained constant along the proximal
urethra, while sympathetic nerves showed a significant
increase along a proximal-distal gradient. Administration
of 17ß-estradiol for 7 days via subcutaneous osmotic
pump did not change smooth muscle area in sections,
and neither densities nor total innervation of any nerve
population was altered.
These findings reveal a rich cholinergic innervation
of the proximal urethra, and a pronounced gradient in
sympathetic innervation. Unlike the embryologically
similar uterine smooth muscle, estrogen does not
influence muscle size or composition of innervation,
indicating that estrogen’s actions on innervation are
highly target-specific. Thus, estrogen’s effects on urinary
continence apparently occur independently of any
significant remodeling of smooth muscle or resident
innervation.
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