Effects of clonidine, a Gi protein-coupled α2-adrenergic receptor agonist, in rats with polycystic kidney disease

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Abstract Title *

Effects of clonidine, a Gi protein-coupled α2-adrenergic receptor agonist, in rats with polycystic kidney disease

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Co-author 1

Takahiro Miura takamiur@gmail.com Tohoku University Graduate School of Medicine Department of Rehabilitation Medicine Sendai Japan *

Co-author 2

Jiahe Qiu jiaheeqiu@gmail.com Tohoku University Graduate School of Medicine Department of Rehabilitation Medicine Sendai Japan -

Co-author 3

Lusi Xu jyolx@yahoo.co.jp ohoku Medical Pharmaceutical University Division of General Medicine and Rehabilitation Sendai Japan -

Co-author 4

Takuo Hirose hirose-t@tohoku-mpu.ac.jp ohoku Medical Pharmaceutical University Division of Nephrology and Hypertension Sendai Japan -

Co-author 5

Takefumi Mori tmori@tohoku-mpu.ac.jp ohoku Medical Pharmaceutical University Division of Nephrology and Hypertension Sendai Japan -

Co-author 6

Osamu Ito oito@hosp.tohoku-mpu.ac.jp ohoku Medical Pharmaceutical University Division of General Medicine and Rehabilitation Sendai Japan -

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Co-author 11

Co-author 12

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Co-author 15

Introduction

While Gs protein-coupled vasopressin type 2 receptor antagonists are used to treat autosomal dominant polycystic kidney disease (ADPKD), Gi protein-coupled somatostatin receptor agonists have not yet been used clinically due to adverse effects and insufficient efficacy. In this study, we investigated the effects of clonidine, a Gi protein-coupled α2-adrenergic receptor (AR) agonist, in PCK rats, an ADPKD model.

Methods

Six-week-old male PCK rats were divided into a control group and a clonidine group. The clonidine group was orally administered clonidine for 12 weeks and its effects were examined.

Results

Clonidine did not increase urine volume but reduced urinary protein. Clonidine slightly increased plasma creatinine but did not affect glomerular sclerosis. It suppressed glomerular epithelial injury, renal cyst growth, and pericystic cell proliferation. Clonidine reduced renal cAMP content and inhibited B-Raf expression, extracellular signal-regulated kinase (ERK), and S6 phosphorylation, but did not affect mammalian target of rapamycin (mTOR) or S6K1 phosphorylation.

Conclusion

In PCK rats, α2AR agonists suppress renal cyst growth without increasing urinary volume, and the mechanism behind this is related to inhibition of the cAMP/B-Raf/ERK/S6 pathway. α2AR agonists may be novel therapeutic agents for ADPKD.

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