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01.12.2015 | Research article | Ausgabe 1/2015 Open Access

BMC Urology 1/2015

Expression of parathyroid hormone/parathyroid hormone-related peptide receptor 1 in normal and diseased bladder detrusor muscles: a clinico-pathological study

BMC Urology > Ausgabe 1/2015
Nobuyuki Nishikawa, Rie Yago, Yuichiro Yamazaki, Hiromitsu Negoro, Mari Suzuki, Masaaki Imamura, Yoshinobu Toda, Kazunari Tanabe, Osamu Ogawa, Akihiro Kanematsu
Wichtige Hinweise

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

NN and AK participated in the design of the study, evaluated the samples, and performed the analysis. NN drafted the manuscript. YT carried out the immunohistochemical study, and helped to draft the manuscript. RY, YY, MS, and KT provided the clinical samples and clinical data, and YY performed the urodynamic study. HN and MI critically reviewed the manuscript. OO conceived of the study, and participated in its coordination. All authors read and approved the final manuscript.



To investigate the expression of parathyroid hormone (PTH)/PTH-related peptide (PTHrP) receptor 1 (PTH1R) in clinical specimens of normal and diseased bladders. PTHrP is a unique stretch-induced endogenous detrusor relaxant that functions via PTH1R. We hypothesized that suppression of this axis could be involved in the pathogenesis of bladder disease.


PTH1R expression in clinical samples was examined by immunohistochemistry. Normal kidney tissue from a patient with renal cancer and bladder specimens from patients undergoing ureteral reimplantation for vesicoureteral reflux or partial cystectomy for urachal cyst were examined as normal control organs. These were compared with 13 diseased bladder specimens from patients undergoing bladder augmentation. The augmentation patients ranged from 8 to 31 years old (median 15 years), including 9 males and 4 females. Seven patients had spinal disorders, 3 had posterior urethral valves and 3 non-neurogenic neurogenic bladders (Hinman syndrome).


Renal tubules, detrusor muscle and blood vessels in normal control bladders stained positive for PTH1R. According to preoperative urodynamic studies of augmentation patients, the median percent bladder capacity compared with the age-standard was 43.6% (range 1.5–86.6%), median intravesical pressure at maximal capacity was 30 cmH2O (range 10–107 cmH2O), and median compliance was 3.93 ml/cmH2O (range 0.05–30.3 ml/cmH2O). Detrusor overactivity was observed in five cases (38.5%). All augmented bladders showed negative stainings in PTH1R expression in the detrusor tissue, but positive staining of blood vessels in majority of the cases.


Downregulation of PTH1R may be involved in the pathogenesis of human end-stage bladder disease requiring augmentation.
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