There have been few studies regarding the onset of urinary sensations and frequent urination induced by sudden whole-body cooling. In this article, we review the relationship between cold stress and urinary frequency based mainly on our previous studies. A recent study showed that cold stress induces bladder overactivity in conscious rats, and these effects were mediated, at least in part, by α1A -adrenergic receptor (AR) and α1D -AR. Another study suggested that the resiniferatoxin-sensitive nerves present in the urinary bladder may also be involved in the regulation of detrusor activity associated with cold stress. The mammalian transient receptor potential (TRP) channel family consists of 28 channels subdivided into five different classes: TRPV (vanilloid), TRPC (canonical), TRPM (melastatin), TRPML (mucolipin), and TRPA (ankyrin). TRP channels function as multifunctional sensors at the cellular level. They can be activated by physical (voltage, heat, cold, mechanical stress) or chemical stimuli and binding of specific ligands. In 2002, it was reported that a nonselective cation channel, TRPM8, could be activated by both menthol and thermal stimuli (8-28 °C). We demonstrated the presence of TRPM8 in the skin from the legs and back of rats by immunofluorescence staining and that stimulation of this receptor by menthol causes urinary frequency. There have been other reports demonstrating roles of TRPM8 not related to its thermosensory function. Further studies are needed to clarify the mechanism of cold stress-induced urinary frequency, and the roles of TRPM8 in the micturition control system.
Keywords: alpha1 adrenergic receptor blocker; benign prostatic hyperplasia; cold stress; lower urinary tract symptoms.
© 2012 Blackwell Publishing Asia Pty Ltd.