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Abstract

Volume 12, Issue 4 (July 2010) 12, 599–604; 10.1038/aja.2009.97

Reduced expression of SK3 and IK1 channel proteins in the cavernous tissue of diabetic rats

Jin-Hai Zhu1, Rui-Peng Jia1, Lu-Wei Xu1, Jian-Ping Wu1, Zi-Zheng Wang2, Shu-Kui Wang2 and Cheng-Jia Bo1

1 Department of Urology, Nanjing First Hospital Affiliated to Nanjing Medical University, Nanjing 210006, China
2 Laboratory of Molecular Medicine, Nanjing First Hospital Affiliated to Nanjing Medical University, Nanjing 210006, China

Correspondence: Dr Rui-Peng Jia,jiaruipengnj@msn.com

Received 1 November 2009; Revised 17 December 2009; Accepted 2 February 2010; Published online 5 April 2010.

Abstract

The small (SK3) and intermediate (IK1) conductance calcium-activated potassium channels could have key roles in the endothelium-dependent hyperpolarization factor pathway, which is believed to contribute to normal penile erection function. We aimed to investigate the expression of SK3 and IK1 in diabetic rodents. The experimental diabetes model was induced in 8-week-old male Sprague–Dawley rats (250–300 g) by a single administration of streptozotocin. Both the diabetes mellitus group (DM group, n = 20) and the control group (NDM group, n = 10) were injected with a low dose of apomorphine to allow for the measurement and comparison of the corresponding penile erections. The mRNA and protein expression levels of SK3 and IK1 were measured by reverse transcription polymerase chain reaction and western blot, respectively. Erectile function was significantly decreased in the DM group compared with control group (P < 0.05). The mRNA and protein expression levels of SK3 and IK1 were reduced in the cavernous tissue of diabetic rats compared with the control group (P < 0.05). Diabetes inhibits mRNA and protein expression of both SK3 and IK1 in the cavernous tissue of diabetic rats. This could play a key role in the development of erectile dysfunction in diabetic rats.

Keywords: diabetes mellitus; endothelium-dependent; hyperpolarization factor; erectile dysfunction; IK1; SK3

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