The Roles of β-Adrenergic Receptor Blockers in Interstitial Cystitis.

Interstitial cystitis (IC) is a debilitating disease characterized by chronic inflammation of the urinary bladder. β-Adrenergic receptor blockers appear to have a beneficial clinical effect in IC. In this paper, we review the evidence of an association between β-adrenergic receptor blockade and IC. The information was obtained from MEDLINE. Genetic studies have provided the opportunity to determine which proteins link β-adrenergic receptor blockade to IC pathology. In particular, this link involves the major histocompatibility complex class II molecules, the renin-angiotensin system, the transcription factor nuclear factor-κB, the nerve growth factor, and the vascular endothelial growth factor. Β-Adrenergic receptor blockers also exert anti-IC effects through non-genomic factors, including stress, mitogen-activated protein kinase pathways, prostaglandins, cyclooxygenase-2, oxidative stress, and nitric oxide synthase. In conclusion, β-adrenergic receptor blockade may play a beneficial role in IC treatment. Additional investigations that examine β-adrenergic receptor blockers as IC therapeutics are required to further elucidate this role.

The Beneficial Role of Vitamin D in Interstitial Cystitis.

Interstitial cystitis (IC) is a poorly understood chronic bladder disorder that is generally characterized by bladder discomfort and increased urination urgency and frequency. Vitamin D levels are associated with bladder pathology, and both rat and human bladders express receptors for vitamin D3. Vitamin D significantly reduced edema and bladder wall leukocyte infiltration in a IC animal model. Genetic studies have provided the opportunity to determine which proteins link vitamin D to IC pathology (i.e., the major histocompatibility complex (MHC) class II molecules, the transcription factor nuclear factor kappa B (NF-κB), RANTES (regulated on activation, normal T cell expressed and secreted), epidermal growth factor (EGF), transforming growth factor beta (TGF-β) family, and vascular endothelial growth factor (VEGF)). Vitamin D also exerts its effect on IC through non-genomic factors, i.e., Bacillus Calmette-Guérin (BCG) vaccination, mast cells and histamine, prostaglandins (PGs), reactive oxygen species (ROS), and inducible nitric oxide synthase (iNOS). Conclusion: Vitamin D may have a beneficial role in IC. Calcitriol is best used for IC because it is the active form of the vitamin D3 metabolite, and it modulates inflammatory cytokine expression. Further investigation with calcitriol in IC patients is needed.