OAB is considered to be one kind of abnormalities in bladder
function. However, neural reflex might take potential and
important part in OAB initiation. The organs neighbored
with the bladder, such as the prostate, the rectum, the female
reproductive system and the pelvic floor muscles, might
influence the bladder excitation through the nerve-nerve
interaction. As we know, the patients with prostatitis always
suffer the voiding dysfunction, probably via an autonomic nerve
reflex. Simultaneously, inflammation in chronic cervicitis can
also bring excitation variation in bladder function. Among these
mechanisms, the psychological, neurogenical and/or myogenical
factors are thought to be involved.
I. Pelvic nerves and LUTS
(I) Prostatitis and voiding dysfunctions
Posterior urethral infections were traditionally considered to be
the main cause for voiding dysfunction. Our results revealed that
the block in the peri-prostate nerves can reduce the reaction of
the bladder function to the prostatitis, which hints that a "visceral
reflex" between the prostate and the bladder. Further study with
PI/Bb double-labeled fluorescence confirmed this result.
(II) Chronic cervicitis and bladder functions
Our studies in animal model revealed that the gynecological
infection electrically diffused, with neural factors involved. Nerve
tract technique revealed that the bladder and the cervix uteri
were innervated by the same neuron, which hinted an "axonaxon
reflex" between the bladder and the uteri.
(III) Rectum and voiding
OAB often combined with constipation. Besides the
psychological influence, Is there any other mechanism involved?
Studies on animals revealed that the constipation can cause
voiding dysfunctions, including the reduce of bladder volume,
increase of the detrusor pressure, and occurrence of the detrusor
II. Neurogeni/ myogenic factors in bladder instability
The traditional hypothesis to explain the detrusor instability
is the supersensitivity of autonomic nerves. How about other
(I) Detrusor spontaneous excitation
Detrusor owes the capability to contract independent to M and
β cholinergic receptors, which was also confirmed in the studies
on VIP and purine receptors.
(II) Stretch load and detrusor excitation
Stretch load can induce the bladder excitation. Over-tension
and permanent stretch load can cause uncontrollable bladder
excitation, which seems to be independent to the innervation.
(III) Whole-bladder study
The whole-bladder can contract in vitro. There seems to be no
distinguish in this kind of whole-bladder contraction between
the neurogenic and obstructive instability.
III. Psychological behaviors and bladder excitation
Sympathetic skin reflex (SSR) was found to be high concord
with the bladder sensory function. SSR might be a good and
objective parameter for indicating the bladder sensory for
normal, oversensitive, hyposensitive, and OAB patients.
IV. Bladder pacemaking and pacemaker
Pacemaking current, higher excitation and unobstructed
transmission are the basic conditions for pacemaking. Bladder
interstitial of Cajal cell behaves as the pacemaking cell in some
kind of degree. Studies showed:
(I) It owes the simultaneous physiological characteristics, and
positive for c-kit dye.
(II) Bladder ICC contains the capabilities of spontaneous
and post-stretch excitation. iii) Excitation can transmit from
ICC to the detrusor myocytes by fluorescence recovery after
phtobleaching (FRAP) studies.
(III) Bladder ICC changed in detrusor instatilities.
(V) c-kit blocker, Glivec can reduce the bladder constriction.