1. ¹Department of Pharmacology, Faculty of Medical Sciences, UNICAMP, Campinas, Sao Paulo, Brazil
2. ²Department of Physical Education, Institute of Bioscience, UNESP, Rio Claro, Sao Paulo, Brazil

Correspondence: Dr A Zanesco, Department of Physical Education, Institute of Bioscience, UNESP, AV 24A, 1515, Rio Claro, Sao Paulo 13506-900, Brazil. E-mail: azanesco@rc.unesp.br

Received 12 March 2006; Revised 19 May 2006; Accepted 29 June 2006; Published online 17 August 2006.

Abstract

The aim of this work was to evaluate the influence of run training on the responsiveness of corpus cavernosum (CC) from rats made hypertensive by treatment with nitric oxide (NO) synthesis inhibitor. Wistar rats were divided into sedentary control (C-SD), exercise training (C-TR), N-nitro-L-arginine methyl ester (L-NAME) sedentary (LN-SD) and L-NAME trained (LN-TR) groups. The run training program consisted in 8 weeks in a treadmill, 5 days/week, each session lasted 60 min. L-NAME treatment (2 and 10 mg/rat/day) started after 4 weeks of prior physical conditioning and lasted 4 weeks. Concentration–response curves were obtained for acetylcholine (ACh), sodium nitroprusside (SNP), sildenafil and BAY 41-2272. The effect of electrical field stimulation (EFS) on the relaxations responses of CC was evaluated. Run training prevented the arterial hypertension induced by L-NAME treatment (LN-SD: 1352 and 1412 mm Hg for both doses of L-NAME) compared to LN-SD groups (1541 and 1752 mm Hg, for 2 and 10 mg of L-NAME, respectively). Run training produced an increase in the maximal responses (E_max) of CC for ACh (C-SD: 473; C-TR: 521; and LN-TR: 533%) and SNP (C-SD: 891; C-TR: 981; and LN-TR: 951%). Both potency and E_max for ACh were reduced in a dose of 10 mg of L-NAME, and run training restored the reduction of E_max for ACh. No changes were found for BAY 41-2271 and sildenafil. Relaxing responses to EFS was reduced by L-NAME treatment that was restored by prior physical conditioning. In conclusion, our study shows a beneficial effect of prior physical conditioning on the impaired CC relaxing responses in rats made hypertensive by chronic NO blockade.