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D. Yilmaz Oral, E. Kaya, E. Yilmaz, N. Bayatli, T. Cengiz, I. Ozakca, S. Gur, PS-04-006 The Beneficial Effect of Hydrogen Sulfide Donor, Sodium Hydrosulfide on Erectile Dysfunction in l-Name-Induced Hypertensive Rats, The Journal of Sexual Medicine, Volume 14, Issue Supplement_4a, April 2017, Pages e117–e118, https://doi.org/10.1016/j.jsxm.2017.03.103
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Objective
Hypertension is a risk factor for erectile dysfunction (ED). Hydrogen sulfide (H2S, an endogenous gasotransmitter) induces smooth muscle relaxation and exerts anti-inflammatory activity. This study investigated the effect of a H2S donor (sodium hydrosulfide, NaHS) on ED in hypertensive rats.
Methods
Adult male Sprague-Dawley rats were divided into 4 groups: control, NaHS (20μM/L)-treated control, Nω-Nitro-L-arginine-methyl ester hydrochloride (L-NAME, 40 mg/rat/day) and NaHS-treated L-NAME. Both treatments were given to rats in the drinking water. The erectile response was expressed as a ratio of intracavernosal pressure (ICP)/mean arterial pressure (MAP). The isometric tension of corpus cavernosum (CC) was measured in organ-bath experiments. The protein expression of inflammatory markers and the smooth muscle/collagen ratio were determined by Western blotting and Masson's trichrome staining.
Results
The blood pressure was significantly increased in the hypertensive group (140.01±5.70 mmHg, p<0.01) compared to the control group (100.30±0.01 mmHg). The treatment failed to reverse the blood pressure in hypertensive rats (139.80±6.10 mmHg, p<0.01). The erectile response in the hypertensive group (0.12±0.01, p<0.001) was remarkably lower than in the control group (0.56±0.02), which was partially improved by NaHS treatment (0.31±0.08, p<0.05). Electrical field stimulation (EFS)-induced and endothelium-dependent relaxation was reduced, while contractile responses to EFS and phenylephrine were not altered in CC from hypertensive rats. Treatment with NaHS restored the nitrergic response in hypertensive rats. The smooth muscle/collagen ratio was partially recovered by the treatment. The expression of nuclear factor kappa B (NF-κB) and NF-κB inhibitor (known as inhibitor kappa B alpha, IκBα) was increased in hypertensive rats. The treatment decreased relatively the expression of NF-κB protein in hypertensive rats.
