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Effects of hydrogen sulphide donor, sodium hydrosulphide treatment on the erectile dysfunction in L‐NAME‐induced hypertensive rats
Author(s) -
Yilmaz Enis,
KayaSezginer Ecem,
YilmazOral Didem,
Cengiz Tugba,
Bayatli Nur,
Gur Serap
Publication year - 2019
Publication title -
andrologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.633
H-Index - 59
eISSN - 1439-0272
pISSN - 0303-4569
DOI - 10.1111/and.13240
Subject(s) - enos , erectile dysfunction , endocrinology , medicine , nitric oxide synthase , fibrosis , cystathionine beta synthase , nitric oxide , vasodilation , blood pressure , chemistry , enzyme , biochemistry , cysteine
Men with hypertension often develop erectile dysfunction (ED). The present study aimed to examine the effects of sodium hydrosulphide (NaHS), a hydrogen (H 2 S) donor, treatment on ED in nitric oxide synthase (NOS) inhibitor (L‐NAME)‐induced hypertensive rats. Forty adult Sprague‐Dawley rats were divided into four groups: control, NaHS (0.037 mg kg day −1 )‐treated control, L‐NAME‐induced hypertension (40 mg kg day −1 ) and NaHS‐treated L‐NAME‐induced hypertension. The ratio of intracavernosal pressure to mean arterial pressure and isometric tension of corpus cavernosum (CC) were measured. The penile expression of endothelial and neuronal NOS (eNOS and nNOS), inflammation markers [nuclear factor kappa B (NF‐κB) and inhibitor kappa B alpha (IκBα)], H 2 S‐producing enzymes[cystathionine β‐synthase (CBS) and cystathionine γ‐lyase (CSE)], the smooth muscle/collagen ratio and H 2 S concentrations were determined. The blood pressure was significantly increased in the hypertensive group, but not reversed by NaHS. The erectile response in hypertensive rats was partially prevented by NaHS. The relaxation response to electrical field stimulation was increased in CC from NaHS‐treated hypertensive rats. NaHS treatment restored decreased protein expression of eNOS, nNOS and CSE as well as smooth muscle/collagen ratio and H 2 S levels and increased NF‐κB and IκBα protein expression in the penile tissue of hypertensive rats. NaHS promoted the recovery of erectile responses in hypertensive rats by improvement of neuronal function and downregulation of fibrosis and NF‐κB signalling.