The internal urethral sphincter is not an anatomically discrete muscle but rather a functional thickening of the circular smooth muscle of the bladder neck and proximal urethra. In males it is well-defined and plays a critical role in preventing retrograde ejaculation; in females it is less prominent. Under sympathetic control (alpha-adrenergic), it maintains closure during bladder filling and is a primary factor in maintaining urinary continence.
| Origin | Circular smooth muscle of the bladder neck and proximal urethra |
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| Insertion | Encircles the bladder neck and proximal urethra as a thickened smooth muscle ring |
| Nerve Supply | Sympathetic fibres from L1-L2 (via hypogastric nerves), stimulation causes contraction and bladder neck closure |
| Blood Supply | Inferior vesical artery; Internal pudendal artery |
| Actions | Involuntary closure of the bladder neck during bladder filling and ejaculation |
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The internal urethral sphincter is the primary structure damaged by alpha-1 blockers used in benign prostatic hyperplasia treatment: these drugs relax the smooth muscle of the bladder neck and prostate capsule, improving urine flow but causing retrograde ejaculation. In men, the internal sphincter is also damaged by transurethral resection of the prostate (TURP) and radical prostatectomy, producing stress incontinence that relies entirely on the intact external (striated) urethral sphincter. Bladder neck contracture after TURP produces outlet obstruction.
Not directly palpable; assessed by urodynamics including videourodynamics showing bladder neck opening during voiding.
Radical prostatectomy disrupts the internal urethral sphincter at the bladder neck, leaving continence dependent solely on the external striated sphincter and pelvic floor; recovery of continence over 3-12 months depends on external sphincter preservation, with severe persistent incontinence managed by artificial urinary sphincter implantation.
Alpha-1 adrenergic blockade relaxes the internal urethral sphincter at the bladder neck, preventing its closure during ejaculation and causing semen to flow retrogradely into the bladder, a predictable side effect of tamsulosin and silodosin treatment for benign prostatic hyperplasia.
