Autonomic nervous control of the urinary bladder

Abstract

The autonomic nervous system plays an important role in the regulation of the urinary bladder function. Under physiological circumstances, noradrenaline, acting mainly on β(3) -adrenoceptors in the detrusor and on α(1) (A) -adrenoceptors in the bladder outflow tract, promotes urine storage, whereas neuronally released acetylcholine acting mainly on M(3) receptors promotes bladder emptying. Under pathophysiological conditions, however, this system may change in several ways. Firstly, there may be plasticity at the levels of innervation and receptor expression and function. Secondly, non-neuronal acetylcholine synthesis and release from the urothelium may occur during the storage phase, leading to a concomitant exposure of detrusor smooth muscle, urothelium and afferent nerves to acetylcholine and noradrenaline. This can cause interactions between the adrenergic and cholinergic system, which have been studied mostly at the post-junctional smooth muscle level until now. The implications of such plasticity are being discussed.

Novel mechanism of hydrogen sulfide-induced guinea pig urinary bladder smooth muscle contraction: role of BK channels and cholinergic neurotransmission

“…The relative contributions of cholinergic and purinergic pathways to DSM voiding contractions appear to vary depending on the species and disease states under pathophysiological conditions (2). ACh is considered to play the primary excitatory role for physiological bladder contraction (7,34). In our study, the blockade of mAChRs with atropine significantly reduced the stimulatory effect of GYY4137 on DSM spontaneous phasic contractions suggesting that H 2 S increases DSM contractility in a mAChR-dependent manner (Fig.…”

“…Activation of mAChRs by ACh plays a key role in triggering bladder voiding contractions (7,34). Therefore, we next investigated whether mAChRs are involved in the GYY4137-evoked DSM contractions.…”

“…neurotransmitter triggering DSM voiding contractions (7,34). In experimental animals and humans, activation of muscarinic ACh receptors (mAChRs) depolarizes the DSM cell membrane potential, enhances action potential generation, promotes influx of Ca 2ϩ via L-type voltage-gated Ca 2ϩ (Ca V ) channels, and leads to increased DSM contractility (6,14,41).…”

The Non-Neuronal Cholinergic System in Health and Disease

“…Bladder outlet obstruction is characterized by an intravesical outlet obstruction that is often associated with detrusor overactivity and dramatic growth responses of muscles and ganglion cells through hyperplasia and hypertrophy (reviewed in Ochodnicky et al [142]). Recently, the NNCS was shown not to be regulated on the mRNA level in this disease [143] whereas a downregulation was measured for the neuronal nAChR subunits α 10 and α 5 (dorsal root ganglia L5-S2) [144].…”

“…Further, a mutation of the M3 mAChR is associated with the onset of bladder outlet obstruction [145]. However, the plasticity at the level of innervation leads to the assumption that the autonomic nervous system is most involved in bladder outlet obstruction, eventually in interaction with the NNCS [142]. …”