![]() ![]() This activates parasympathetic and inhibit sympathetic outflow. Increasing urine volume will increase the frequency of afferent impulses, which in turn will shift efferent signaling from the pontine storage to the micturition center. The somatic nerves also participate in the process of increasing bladder outlet resistance by releasing acetylcholine. Released norepinephrine induces detrusor relaxation and enhances bladder compliance, which is mediated largely through β 3-adrenergic receptors, while bladder outlet resistance is enhanced by activation of α 1-adrenergic receptors in the bladder neck, urethra and prostate (Michel and Vrydag, 2006). For many years, it was considered as a passive barrier for the passage of ions and solutes, but currently is known to possess a number of novel features that allow it to respond to various physical and chemical stimuli, resulting in the release of various substances from the urothelial cells: these include ATP, nitric oxide (NO), substance P, acetylcholine, adenosine, antiproliferative factor, cytokines, various trophic factors, and prostanoids (Birder and de Groat, 2007).ĭuring bladder filling at low volumes, low frequency impulses activate afferent nerves to signal the pontine storage and micturition centers, and stimulate sympathetic outflow via hypogastric and pudendal nerves. The urothelium represents the layer of epithelial cells lining the urinary tract between the renal pelvis and the urinary bladder. The molecular basis of distention sensing has not been fully clarified, but may involve the urothelium as a major factor during this process. Increasing the volume of the urinary bladder provokes afferent signals to the central nervous system. Micturition is a highly coordinated process that starts with sensing bladder filling, transferring data to the central nervous system processing center and efferent pathways resulting in the voiding response.
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