Adrenoceptors importantly contribute to the physiological regulation of lower urinary tract (LUT) function and have become a target of several clinically successful treatments for major LUT diseases. In the bladder dome, β-adrenoceptor subtypes are found in multiple cell types and mediate relaxation of detrusor smooth muscle, perhaps partly indirectly by acting on afferent nerves and cells of the mucosa. β 3 -adrenoceptor agonists such as mirabegron and vibegron are used to treat overactive bladder syndrome. In the bladder trigone and urethra, α 1 -adrenoceptors cause contraction and thereby physiologically contribute to bladder outlet resistance. α 1 -adrenoceptors in the prostate also cause contraction and pathophysiologically elevate bladder outlet resistance leading to voiding dysfunction in benign prostatic hyperplasia. α 1 -adrenoceptor antagonist such as tamsulosin is widely used as a first-line option to treat LUT symptoms in men, but it remains unclear to which extent and how smooth muscle relaxation contributes to symptom relief.
Keyphrases
- urinary tract
- smooth muscle
- benign prostatic hyperplasia
- lower urinary tract symptoms
- prostate cancer
- induced apoptosis
- spinal cord injury
- oxidative stress
- single cell
- cell cycle arrest
- stem cells
- physical activity
- cell proliferation
- cell death
- depressive symptoms
- signaling pathway
- case report
- endoplasmic reticulum stress
- botulinum toxin