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Potent endonthelial‐independent relaxation promoted by a nitrosyl ruthenium complex in rabbit aorta and corpora cavernosa
Author(s) -
Fonteles Manassés Claudino,
Cerqueira João Batista Gadelha,
Sousa Clauber Mota,
Alencar Cunha Karina Moreira,
Lopes Luiz Gonzaga França,
Sousa Moreira Ìcaro,
Nascimento Nilberto Robson Falcão
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.916.2
Subject(s) - iberiotoxin , glibenclamide , apamin , phenylephrine , sodium nitroprusside , chemistry , vasodilation , enos , ruthenium red , endocrinology , nitric oxide , pharmacology , potassium channel , medicine , nitric oxide synthase , blood pressure , calcium , diabetes mellitus , organic chemistry
Nitric oxide (NO) is a key mediator of both vasodilation and penile erection. Some metal nitrosyl complexes are being tested as NO donors. The current work compared LLNO1 a nitrosyl ruthenium complex to sodium nitroprusside (SNP). The tissues were mounted in organ baths for isometric recordings, precontracted with 1 μ M phenylephrine and concentration‐response curves (10 −11 a 10 −4 M) to LLNO1 were obtained. In order to investigate the mechanisms involved, oxyhemoglobin (10μM), L‐cysteine (1 mM), glibenclamide (100 μ M .) or iberiotoxin (1 μM) plus apamin (0,1 μM) were added 30 minutes before LLNO1 curves in separate protocols. LLNO1 completely relaxed phenylephrine‐contracted aortic rings with PD 2 of 4.8 [5‐4.5] compared with a Rmax of 100% and PD 2 of 5.8[6.3‐5.2] to SNP. This effect was partially blocked by oxyhemoglobin with Rmax reduced to 34.6±3.8% and PD 2 [4.3[4.8‐3.9]. The corpora cavernosa strips were also relaxed by LLNO1 with Rmax of 72.6±6.6% and PD 2 of 5.9[6.5‐5.3]. Similarly, this relaxation was blocked in 73% by pre‐treating the tissues with oxyhemoglobin. The incubation of tissues during 30 min with L‐cysteine, glibenclamide or iberiotoxin+apamin did not change the effect of LLNO1 in any of the tissues studied. LLNO1 is a potent aortic vasodilator and corpora cavernosa relaxant agent that acts predominatly by releasing NO and with no significant nytroxyl releasing properties.