Physiology of micturition

In very young children micturition has no circadian rhythm. A circadian rhythm with daily micturition and absence of nocturia (nightly vasopressin peak) will slowly assert itself during childhood and usually be mostly set by three years of age. Sporadical nocturia may though continue to occur for a few years. This situation is the essentially stable until old age. So it may safely be assumed that you should be able to undisturbed sleep for 6-8 hours and not need to immediately rush to micturate as soon as you wake up. (And certainly not to suddenly feel an overwhelming and even painful need to immediately micturate.) Normal average 24 hour diuresis is 1600 +/- 350 ml. Daytime average diuresis is about 1100 +/- 250 ml at age 30 and slightly lower in older people, about 800 +/- 150 ml.(1) (These figures vary somewhat and e.g. Raman et al. calculated 2200 ml as average normal diuresis.(2))

A healthy subject needs about 50 ml of liquid in the bladder, after a complete voiding, for some feeling of fullness. At about approximately 200 ml desire of voiding should start to occur, after which sensations of discomfort increase. At about 400 ml a strong urge to urinate is normally forcing an individual to void. (Stretch receptors in the detrusor signal the CNS, which leads to relaxation of the bladder neck, trigone, and urethra muscles.) During the day you should thus not need to micturate more than 3-5 times. Intervals between voidings should be longer than 2
hours with no feelings of urgency. (It should be noted that the Incontinence Society regards more than 8 voidings per 24 hours as an abnormal frequency a.k.a. an "overactive bladder".(3))

Regulation of micturition is very complex. It is an interplay between the HPA axis, the Pontine micturition center and neurological feedback from the bladder and pelvic floor. The bladder (detrusor muscle) is innervated by hypogastric (sympathetic nervous system) nerve fibres from the lumbar spinal region (control of storage) and pelvic (parasympathetic) nerve fibres from the sacral spinal region (to the ‘detrusor pelvic plexus’; control of voiding). Urethral smooth longitudinal and circular muscle are also innervated by hypogastric nerve fibres. The striated muscle of the urethral sphincter by pudendal nerve (somatic motor) fibres from the sacral spinal region. And the striated muscle of the pelvic floor by sacral nerve (somatic motor) fibres. The somatic fibres are involved in volitional micturition control (i.e. is under your "voluntary" control). Additional detail can be found in references 4-7.

Bladder filling is regulated by water homeostasis, especially the regulation of electrolyte levels (and then especially sodium) and blood volume (to avoid hypovolemia). This is in turn regulated by the release of vasopressin (AVP) and it’s binding to the type-2 receptor in renal principal cells. AVP production is regulated by specific regions of the hypothalamus and release by the pituitary. Regulation of AVP levels is also dependant on various hormones (PGE-2, bradykinin, dopamine, EGF etc). Vasopressin maximum occurs normally between approximately 1900 and 0700 hours. Nocturia may occure due to a shift of this interval.

Do notice that prostaglandin E2 levels are affected by many of the CPPS treatments, which may explaine their beneficial effect on diuresis/water balance (stimulates diuresis in the absence of AVP, otherwise it counteracts it). A full review of the current understanding can be found in Boone and Deen.(8)

A recent murine study (9) showed that partial bladder obstruction induced neurological sequelae (through locus coeruleus hyperactivity). It would have been interesting if the authors also had reported sleep patterns and changes in behaviour, to clarify if the causality was due to bladder distension or sleep disruption. Animal studies have shown that reduced serotonin levels trigger increased urinary frequency and detrusor overactivity. And in Europe duloxetine, a serotonin
norepinephrine reuptake inhibitor (anti-depressant) is approved for treatment of incontinence. A controversial treatment due to its adverse effects.

The "Musculo-Elastic Theory of anorectal function and dysfunction in the female" regarding "suspensory ligaments inactivating anorectal muscle forces" is also interesting as stress incontinence has been cured by surgical reinforcement of damaged ligaments correcting muscular dysfunction. An interesting overview is found in the journal of Pelviperineology.(10)

Andra bloggar om CPPS, kroniskt bäckenbottensmärtsyndrom, kronisk abakteriell prostatit, NIHIIIb, miktionsfysiologi, miktion
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(1) Asplund R. Nokturi och nattlig polyuri bland äldre [Nocturia and nocturnal polyuria in the elderly]. Läkartidningen 99(44):4370-4373, 2002. (In swedish).
(2) Raman A et al. Water turnover in 458 American adults 40-79 yr of age. Am J Physiol Renal Physiol 286: F394-F401, 2004
(3) Overactive bladder. ICS factsheet 2, july 2005.
(4) Andersson K-E, Hedlund P. Pharmacologic perspective on the physiology of the lower urinary tract. Urology 60(suppl 5A):13-21, 2002.
(5) Sugaya K, Nishijima S, Miyazato M, Ogawa Y. Central nervous control of micturition and urine storage. J Smooth Muscle Res 41(3):117-132, 2005.
(6) Birder LA, de Groat WC. Mechanisms of Disease: involvement of the urothelium in bladder dysfunction. Nature Clinical Practice Urology 4:46-54, 2007.
(7) Drake MJ. The Integrative Physiology of the Bladder. Ann R Coll Surg Engl. 89(6):580-585, 2007.
(8) Boone M, Deen PMT. Physiology and pathophysiology of the vasopressin-regulated renal water reabsorption. Eur J Physiol 456:1005-1024, 2008.
(9) Rickenbacher E, Baez MA, Hale L, Leiser SC, Zderic SA, Valentino RJ. Impact of overactive bladder on the brain: central sequelae of a visceral pathology. Proc Natl Acad Sci USA. 105(30):10589-94, 2008.
(10) Pelviperineology Vol 27 N.3 September 2008.