Home  |  Archive  |  Online Submission  |  News & Events  |  Subscribe  |  APFA  |  Society  |  Links  |  Contact Us  |  中文版

Ahead of print
Authors' Accepted
Current Issue
Special Issues
Browse by Category

Manuscript Submission

Online Submission
Online Review
Instruction for Authors
Instruction for Reviewers
English Corner new!

About AJA

About AJA
Editorial Board
Contact Us

Resources & Services

Email alert

Download area

Copyright licence
EndNote style file
Manuscript word template
Guidance for AJA figures
    preparation (in English)

Guidance for AJA figures
    preparation (in Chinese)

Proof-reading for the

AJA Club (in English)
AJA Club (in Chinese)


Societies & Institutes
Databases & Libraries
Other links


Volume 12, Issue 3 (May 2010) 12, 415–421; 10.1038/aja.2009.70

Purinergic contraction of the rat vas deferens in L-NAME-induced hypertension: effect of sildenafil

Serap Gur1, Suresh C. Sikka1, Gillian E. Knight2, Geoffrey Burnstock2 and Wayne J.G. Hellstrom1

1 Department of Urology, Tulane University Health Sciences Center, New Orleans, LA 70112, USA
2 Autonomic Neuroscience Centre, Royal Free and University College Medical School, Rowland Hill Street, London NW3 2PF, UK

Correspondence: Prof. Wayne J.G. Hellstrom, whellst@tulane.edu

Received 6 July 2009; Revised 13 August 2009; Accepted 19 September 2009; Published online 22 March 2010.


Hypertension (HTN) is a risk factor for erectile dysfunction, but its effect on vas deferens (VD) contractility and the ejaculatory response has not been delineated. NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, was used for induction of nitric oxide (NO)-deficient HTN. Our aim was to evaluate the effects of L-NAME-induced HTN on rat VD contractility and to determine whether sildenafil affects VD contractility. A total of 36 male rats were divided into (1) control, (2) L-NAME–HTN, (3) sildenafil treated L-NAME–HTN groups. Group 2 was treated with L-NAME (40 mg kg-1 per day) in drinking water for 4 weeks. Group 3 received sildenafil (1.5 mg kg−1 per day, by oral gavage) concomitantly with L-NAME. The prostatic portion of the VD was subjected to electrical field stimulation (EFS, 1–20 Hz), and the P2X1 agonist α,β-methylene ATP (α,β-meATP, 100 μmol L−1–1 μmol L−1) and the α1-adrenoceptor agonist phenylephrine (Phe, 100 μmol L−1–1 mmol L−1) were used to construct concentration-response curves. These experiments were repeated in the presence of P2X receptor antagonist, pyridoxalphosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS, 30 μmol L−1). VD contractions in response to EFS, α,β-meATP and Phe were significantly enhanced by L-NAME. Sildenafil treatment in the L-NAME group improved the contractile response of VD to EFS (20 Hz). In the presence of PPADS, the enhanced contractile response of VD to EFS and α,β-meATP in hypertensive rats was reversed. In the rat model of chronic NO depletion, the purinergic and adrenergic components and EFS affect VD contractility. The VD contractile response may be mediated more by the purinergic system than the adrenergic system, and sildenafil may alter the ejaculatory response in men with PE.

Keywords: hypertensive rat; NG-nitro-L-arginine methyl ester; purinergic receptors; P2X; sildenafil; vas deferens

PDF | 中文摘要 |

Browse:  609
Copyright 1999-2015    Shanghai Materia Medica, Shanghai Jiao Tong University.    All rights reserved