With regard to a symptom wherein bladder cannot be empty (incomplete bladder emptying) resulting from insufficient micturition contraction, a new terminology of underactive bladder has recently been proposed. 
Underactive bladder is caused by bladder contraction dysfunction, i.e. a clinical condition wherein contractility of the bladder detrusor is decreased (detrusor underactivity), or a combination of urethral relaxation dysfunction (lower urinary tract passage dysfunction), i.e. a clinical condition with insufficient relaxation of the urethral sphincter and bladder contraction dysfunction, which is classified into neurogenic underactive bladder, myogenic underactive bladder, drug-induced underactive bladder, age-related underactive bladder, and underactive bladder induced by other factors (e.g., underactive bladder due to lower urinary tract obstruction, infection and stress etc.)  depending on the causes. 
Examples of causative diseases of neurogenic underactive bladder include: peripheral nerve disorders such as diabetes, disc hernia, spinal canal stenosis, Guillain-Barre syndrome, and herpes zoster-induced peripheral neuritis; spinal cord diseases, for example, supranuclear spinal cord injury, spinal cord tumor, cervical spondylosis, vascular diseases of the spinal cord, spina bifida, myelomeningocele and tethered cord syndrome; and brain diseases, such as dementia, cerebrovascular diseases, Parkinson's disease, spinocerebellar degeneration, olivopontocerebellar atrophy (OPCA), Shy-Drager syndrome, brain tumor, multiple sclerosis, cerebral trauma and encephalitis etc.  In some cases, underactive bladder is caused by surgical injury of pelvic nerve, hypogastric nerve or pudendal nerve controlling voiding functions after surgical operations of pelvic viscera (uterine cancer or rectal cancer). 
The myogenic underactive bladder is largely caused by a cryptogenic decreased activity of the bladder detrusor. 
Examples of drug-induced underactive bladder include underactive bladder developed by anticholinergic drugs, drugs which inhibit release of acetylcholine and other factors. 
Additionally, aged people generally exhibit dysuria caused by weakened bladder activity, and as a result, age-related underactive bladder becomes an important problem in an aging society. 
Other examples of factors which cause underactive bladder include lower urinary tract obstruction caused by prostatic hyperplasia, bladder neck contracture or uterine prolapse, infections such as cystitis and urethritis, and stress (see Non-Patent Documents 1, 2 and 3). 
For the treatment of underactive bladder, drugs which enhance the contractility of the bladder detrusor or reduce urethral resistance through the relaxation of the urethral sphincter are used.  For example, cholinergic agents, such as bethanechol and acetylcholinesterase inhibitors, such as distigmine, are used as drugs for enhancing the contractility of the bladder detrusor.  However, bethanechol also contributes to the contraction of the bladder detrusor at the urine collection period, which causes damage to the urine collection function of the bladder, and at the same time, has side effects such as lacrimation, perspiration, gastrointestinal disorders, abdominal pain etc.  Therefore, it is contraindicated for pregnant women, and patients suffering with peptic ulcer, organic intestinal tract obstruction, asthma, hyperthyroidism etc.  As acetylcholinesterase inhibitors, for example, distigmine and neostigmine, have been used.  Since acetylcholinesterase inhibitors enhance the activity of acetylcholine released from the pelvic nerve endings in urination to enhance the contraction of the bladder detrusor in urination, they are considered excellent drugs when the physiological mechanism of micturition is taken into consideration.  However, since distigmine contracts the bladder detrusor and also causes the contraction of the urethral sphincter due to a potent nicotine-like activity thereof to increase urethral resistance, voiding efficiency is not good and effects in terms of clinical application is insufficient.  Additionally, the risk of high-pressure voiding has also been pointed out (see Non-Patent Document 4). 
As drugs for relaxing the urethral sphincter and reducing urethral resistance, for example, al receptor antagonists, such as tamsulosin, prazosin, alfuzosin, naftopidil, urapidil etc.  have been used and are reported that they are effective for the amelioration of subjective symptoms, such as feeling of residual urine and nocturia.  However, since there are antihypertensive effects including orthostatic hypotension etc.  as a side effect care should be taken for administration thereof.  Additionally, there has been no report demonstrating satisfactory effects on underactive bladder. 
Namely, drugs currently used for the treatment of underactive bladder are not clinically satisfactory in terms of therapeutic effects and safety. 
On the other hand, Patent Document 1 discloses a compound for improving the blood flow in cauda equina nerve tissues, represented by formula (A):

wherein the ring AA represents a 5- or 6-membered cyclic group which may contain 1 to 3 heteroatoms selected from nitrogen, oxygen and sulfur atoms or may further have substituents, XA and YA each independently represent a nitrogen atom or a carbon atom, DA represents a hydrocarbon group which may have substituents, EA represents a bond, an oxygen atom, or a sulfur atom which may be oxidized, GA represents a bond, a hydrocarbon group which may have substituents or a heterocyclic group which may have substituents, JA represents an acidic group which may be protected, and WA represents a hydrocarbon group which may have substituents.  Additionally, it is disclosed that the compound represented by formula (A) is effective for bladder disorder caused by cauda equina compression (see Patent Document 1.). 
Additionally, a compound having a nerve regeneration or protection activity, represented by formula (B):

wherein E1B represents an oxygen atom or a sulfur atom which may be oxidized, RB represents a hydrogen atom or a C1-C8 aliphatic hydrocarbon group, R1B represents a hydrogen atom or a C1-C4 aliphatic hydrocarbon group, and R2B represents a hydrocarbon group which may have substituents is disclosed (see Patent Document 2.). 
The compound of the present invention has not been disclosed in any literature. 
Additionally, it is neither described nor suggested anywhere: the compound of the present invention acts on the bladder detrusor and urethral sphincter to enhance the contractility of the bladder detrusor and relax the urethral sphincter on the other hand; can ameliorate bladder contraction dysfunction or urethral relaxation dysfunction by the both activities; and exhibits effectiveness against underactive bladder, including myogenic, drug-induced, age-related etc.  Additionally, it is neither described nor suggested that the compound of the present invention has little risk of side effects on the urinary system, the circulatory system and the digestive system; and has excellent pharmacokinetics, including oral absorbability, metabolic stability and efficacy duration.