The physiological function of female voiding involves bladder storage and regular voiding through the urethra. The mechanism of voluntary bladder urinary control and voiding is complex and requires normal function of the central and peripheral nervous systems, and normal anatomic location and function of the bladder wall, forceps, urethra, and supporting tissues of the pelvic floor; structural or functional abnormalities in any of these components can lead to abnormal voiding function. The following is a brief overview of normal female voiding physiologic function and associated neurophysiology. 1 Female voiding mechanism 1.1 Bladder storage mechanism in the physiological process of bladder filling, despite the increase in urine volume, but the bladder pressure does not increase, this process is called “bladder adaptive regulation”, mainly due to the smooth muscle and bladder wall connective tissue has passive elastic and viscoelastic properties. When the increase in bladder filling reaches a critical point of intravesical pressure, the contractility of the detrusor muscle is inhibited by activation of the spinal sympathetic reflex, resulting in inhibition of parasympathetic ganglion conduction, which stimulates the β-adrenergic receptors in the bladder body. These factors interact in a network-like fashion during bladder filling and storage of urine, resulting in little or no increase in intraurethral pressure with changes in bladder volume. 1.2 Urethral control mechanisms Because the urethra is located above the anterior vaginal wall, the supporting structures of the anterior vaginal wall directly influence the support of the urethra. The anterior vaginal wall is connected to the pelvic fascial tendon arch, which is formed by the convergence of the anal raphe fascia. It has been found that the complete support of the bladder neck and the adjacent tissues of the retropubic urethra is necessary to maintain urinary control in a stressful state. The support of the urethra by the anterior vaginal wall can be altered by defects in the connection between the vaginal wall and the levator ani muscle at the pelvic fascial tendon arch. One third of the urethral sphincter is a circular muscle that wraps around the lumen of the urethral canal like the anal sphincter, the other female urethral sphincters are the urethral constrictor and the urethrovaginal sphincter. If a woman is able to control her urine on her own, the pressure in the urethra must be higher than the pressure in the bladder, both at rest and under stress conditions. In the resting state, the resistance of the urethra comes from the interaction of urethral smooth muscle, the elasticity and vascular distribution of the urethral wall and the periurethral muscles [1]. 1.3 The role of the anal raphe in urinary control The anal raphe includes the pubococcygeus, iliococcygeus and puborectalis muscles, and of significance for urinary control is the pubococcygeus, which when contracted holds the pelvic floor tightly upward into the pelvis. This action gives the urethra a solid leaning board. Therefore, pelvic floor exercises are used clinically to strengthen the contraction of the levator ani muscle, thereby improving urinary control in women [1]. The anal raphe and periurethral muscles have a dual role in maintaining urinary control, providing resting tension and auxiliary support of the urethra (slow-twitch fibers) on the one hand, and rapid contraction (fast-twitch fibers) in response to increased abdominal pressure on the other. The combined action of these two groups of somatic muscles is essential for normal urinary control. During rapid increases in abdominal pressure and interruptions in urination, the periurethral muscles appear to contract autonomously and reflexively, mainly with increased urethral pressure in the mid and distal urethra. In conclusion, the ability of a woman to control urination properly depends on the interconnection of many different mechanisms. 2 Female voiding-related neurophysiology 2.1 Voiding-related neural pathways The smooth muscles of the bladder are primarily innervated by parasympathetic nerves, whereas those of the urethra and bladder neck are innervated by sympathetic nerves. Branches of the pubic nerves innervate the skeletal muscles in the external urethral sphincter. These nerves are constituted by efferent nerve pathways from the spinal cord to the lower urinary tract. The parasympathetic nerves that innervate the detrusor muscle emanate from sacral 2 to 4 of the spinal cord. As with all parasympathetic nerves, the neurotransmitter of the anterior ganglion is acetylcholine, but the neurotransmitter of the posterior ganglion varies with the target organ. The postganglionic parasympathetic neurotransmitter of the urethral smooth muscle is nitrous oxide, whereas that of the detrusor smooth muscle acts via acetylcholine and adenosine triphosphate. The role of the sympathetic nervous system is to relax the bladder and contract the urethra. Whether or not acetylcholine is apportioned as an anterior ganglionic neurotransmitter in the parasympathetic nervous system, the posterior ganglionic neurotransmitter is norepinephrine. The spinal cord sends sympathetic nerves from thoracic 10 to lumbar 2 to control the bladder, which travels via the posterior ganglia and hypoglossal nerves to the target organs. The somatic nerves afferent to the lower urinary tract are primarily from the pubic nerves, which emanate from sacral 2 to 4 of the spinal cord. The motor neurons of the sacral 2 to 4 segments of the spinal cord are located in Onuf’s nucleus. The neurotransmitter acetylcholine acts in the external urethral sphincter with nicotinic receptors. Parasympathetic, sympathetic, and somatic nerve efferent pathways also serve as relay stations for sensory afferents from the lower urinary tract to the spinal cord and central nervous system. The sensory receptors of the parasympathetic nerve (Aδ and C fibers) transmit both information about bladder capacity during urinary storage and contraction amplitude during voiding. It is suggested that parasympathetic nerves both control the initiation of voiding and maintain bladder contraction during voiding. 2.2 Synergistic reflexes The interaction between the central nervous system and the neural pathways of the lower urinary tract is a synergistic reflex that may be activated on one side and inhibited on the other, e.g. parasympathetic excitation causes contraction of the detrusor muscle followed by relaxation of the urethra, and this reflex inhibits sympathetic activity as well as contraction of the smooth muscle of the urethra controlled by the somatic nerves. 2.3 Bladder storage neurophysiology bladder distension leads to the release of pelvic nerve afferent impulses. Through synapses in the pubic nucleus, pubic nerve efferent impulses cause contraction of the external urethral sphincter. At the same time, sympathetic afferent impulses to the inferior ventral nerve. Via synapses in the sympathetic nucleus, efferent impulses lead to: (i) inhibition of information transmission from posterior parasympathetic ganglion neurons, which inhibits contraction of the detrusor muscle; and (ii) increased tone of the bladder neck. The net effect is that the intraurethral pressure remains higher than the pressure generated by the detrusor muscle, thus favoring urine saving [2]. 2.4 Bladder voiding neurophysiology The pelvic nerve afferent nerves pass up the spinal cord and synapses along the cerebral bridge voiding center. The descending efferent nerve pathway leads to: i) inhibition of pubic nerve impulse transmission, which allows relaxation of the external sphincter; ii) inhibition of sympathetic nerve impulse transmission, which allows bladder neck opening as well as transmission of impulses by parasympathetic postganglionic neurons; and iii) transmission of pelvic parasympathetic impulses, which causes contraction of the detrusor muscle. The result is that the contraction of the detrusor muscle is immediately followed by relaxation of the external urethral sphincter to lower the intraurethral pressure and urination begins. 2.5 Cessation of bladder voiding neurophysiological urine flow is interrupted autonomously. Motor complex synapses in the nucleus accumbens send nerve impulses to the descending corticospinal pathway, resulting in contraction of the external urethral sphincter. At the same time, parasympathetic impulses controlling the contraction of the detrusor muscle are inhibited, while sympathetic activation allows relaxation of the bladder detrusor and contraction of the urethral smooth muscle. The pressure in the urethra is higher than the pressure in the bladder, causing interruption of urine flow. 3 Female urination physiological process When urine is stored in the bladder up to a certain amount, it causes reflex urination and is discharged out of the body through the urethra. Under normal circumstances, the bladder reaches a certain volume and then enters the urinary emptying stage, when the pull receptors feel the signal of bladder distension and fullness and transmit it to the central system, the automatic urination starts at the right time and place called the voiding reflex, this physiological process is an important part of the spinal reflex, and the higher centers can inhibit or strengthen its reflex process. When there is no urine in the bladder, the pressure in the bladder is zero, when the volume of urine in the bladder is 30~50ml, its pressure rises to 5~10cmH2O, when the volume of urine in the bladder is 200~300ml, the increase of pressure in the bladder is not obvious. When the volume of urine in the bladder is >300ml, the pressure in the bladder rises significantly, and the receptors on the bladder wall are excited by the tension stimulation, and the nerve impulses are transmitted along the pelvic nerve afferent fibers to the primary center of the voiding reflex in the sacral segment of the spinal cord, and the impulses are also transmitted to the brainstem and the voiding reflex center in the cerebral cortex to produce the urge to urinate. When the micturition reflex occurs, the efferent signal from the spinal micturition center of the sacral segment is transmitted via the pelvic nerve, causing the contraction of the detrusor muscle and the diastole of the internal urethral sphincter, and the urine is pressed toward the posterior urethra, stimulating the urethral receptors, and the impulse is transmitted again along the pubic nerve to the spinal micturition center of the sacral segment, causing the contraction of the detrusor muscle to increase, the pressure in the bladder to rise, the position of the bladder neck to fall and open in a cone shape, and urination to begin. Brainstem modulation of the voiding reflex causes contraction of the detrusor muscle until the bladder is completely emptied. Normal voiding is an autonomous act that involves reflex-coordinated urethral relaxation and sustained bladder contraction until the bladder is completely empty. In healthy women, the micturition reflex is not a simple segmental sacral reflex but is regulated by the pontine micturition center. The casual control of the voiding reflex is regulated by the connection between the frontal surface of the cerebral cortex and the pons, and the casual control of the external urethral sphincter is exerted through the corticospinal pathway connecting the frontal cortex to the nucleus accumbens in the ventral horn of the sacral spinal cord. In terms of urodynamics, the voiding reflex begins with a sudden and complete relaxation of the urethral and pelvic floor transverse muscles and a decrease in intraurethral pressure. Subsequently, an overall highly coordinated contraction of the detrusor muscle causes an increase in intravesical pressure and the bladder neck and distal urethra begin to descend and form a funnel shape, and voiding begins. Brainstem modulation of the voiding reflex permits contraction of the detrusor muscles long enough to urinate completely. With the voluntary termination of voiding, the urethral and pelvic floor transverse muscles begin to contract and the bladder floor is raised, the intraurethral pressure increases, the forceps is reflexively inhibited, and voiding ends. In conclusion, the physiological process of female voiding is complex, involving pelvic floor anatomical structures such as muscles, ligaments and complex innervation. Only when the physiological mechanism of female urination is properly understood and mastered can various clinical abnormalities in urination be correctly handled.