Mechanisms of action for α1-adrenoceptor blockers in storage symptoms with new insights into the micturition reflex

- α1-blockers suppress micturition reflex.
- α1-blockers modulate symptoms thorough α1A- and α1D-adrenoceptor subtypes in the brain, spinal cord and/or urinary bladder.
- The α1D-adrenoceptor subtype may be more significant than the α1A subtype for inhibiting of the micturition reflex.

Elderly patients suffering from lower urinary tract symptoms with benign prostatic hyperplasia (BPH) are widely prescribed α1-adrenoceptor blockers (α1-blockers) to improve voiding and storage symptoms. The mechanism of action for improvements in voiding symptoms is well understood; tonus of the urethra and prostate are decreased and urinary flow rate is increased by α1-blockers. However, the mechanisms underlying storage symptoms have remained unclear, although detrusor hyperactivity has been identified as a significant factor. Previous investigations have yielded informative results, such as amelioration of reduced blood flow and afferent C-fiber activation, and the importance of the urothelium. Recently, the fascinating role of α1A- and α1D-adrenoceptor subtypes have been investigated for bladder function. Furthermore, the scope of this pathology covers both the bladder and that part of the central nervous system related to the micturition reflex. This review describes the beneficial effects of α1-blockers on storage symptoms and the pathogenesis of storage symptoms related to BPH, discusses the mechanisms of action for α1-blockers with reference to results from cystometry to suggest improvements in management that suppress detrusor hyperactivity, and examines the potential influence of α1A- and α1D-adrenoceptor subtypes on bladder activity.

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