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- Title
Characterization of relaxant mechanism of H<sub>2</sub>S in mouse corpus cavernosum.
- Authors
Aydinoglu, Fatma; Ogulener, Nuran
- Abstract
The aim of this study was to investigate the mechanism of H2S-induced relaxation in mouse corpus cavernosal tissue. l-cysteine (10−6 × 10−3 mol/L) and exogenous H2S (Na HS; 10−6 to 10−3 mol/L) induced concentration-dependent relaxation. l-cysteine-induced relaxations was reduced by d,l-propargylglycine, a cystathionine gamma lyase ( CSE) inhibitor but not influenced by aminooxyacetic acid, a cystathionine beta synthase ( CBS) inhibitor. l-cysteine induced relaxations, but not of those of H2S diminished in endothelium-denuded tissues. N ω-nitro- l-arginine ( l- NA; 10−4 mol/L), a nitric oxide synthase inhibitor, and ODQ (10−4 mol/L), a guanylyl cyclase inhibitor, increased the H2S-induced relaxation. Zaprinast (5 × 10−6 mol/L) and sildenafil (10−6 mol/L), phosphodiesterase inhibitors, inhibited H2S-induced relaxation. Adenylyl cyclase inhibitors N-ethylmaleimide (2.5 × 10−5 mol/L) and SQ22536 (10−4 mol/L) reduced relaxation to H2S. Also, H2S-induced relaxation was reduced by KCl (50 mmol/L), 4-aminopyridine (10−3 mol/L), a Kv inhibitor, glibenclamide (10−5 mol/L), a KATP inhibitor or barium chloride (10−5 mol/L), a KIR inhibitor. However, H2S-induced relaxation was not influenced by apamin (10−6 mol/L), a SKCa2+ inhibitor, charybdotoxin (10−7 mol/L), an IKCa2+ and BKCa2+ inhibitor or combination of apamin and charybdotoxin. Nifedipine (10−6 mol/L), an L-type calcium channel blocker and atropine (10−6 mol/L), a muscarinic receptor blocker, inhibited H2S-induced relaxation. However, H2S-induced relaxation was not influenced by ouabain (10−4 mol/L), a Na+/K+- ATPase inhibitor. This study suggests that H2S endogenously synthesizes from l-cysteine by CSE endothelium-dependent in mouse corpus cavernosum tissue, and exogenous H2S may cause endothelium-independent relaxations via activation of K channels ( KATP channel, KV channels, KIR channels), L-type voltage-gated Ca2+ channels, adenylyl cyclase/ cAMP pathway and muscarinic receptor, and there is the interaction between H2S and NO/ cGMP.
- Subjects
HYDROGEN sulfide; CYSTATHIONINE gamma-lyase; MUSCLE relaxants; ENDOTHELIUM; CYSTATHIONINE beta-synthase; CYSTEINE; PHOSPHODIESTERASE inhibitors
- Publication
Clinical & Experimental Pharmacology & Physiology, 2016, Vol 43, Issue 4, p503
- ISSN
0305-1870
- Publication type
Article
- DOI
10.1111/1440-1681.12554