The ruthenium-based nitric oxide scavenger, AMD6221, augments cardiovascular responsiveness to noradrenaline in rats with streptozotocin-induced diabetes

Hutchings, Simon; Song, Dongzhe; Fricker, Simon P.; Pang, Catherine C.Y.

doi:10.1016/j.ejphar.2005.10.039

Cited by 17 publications

(6 citation statements)

References 15 publications

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“…The low cytotoxic characteristics of ruthenium-derived complexes are well known [59,60]. The trans -[RuCl([15]aneN 4 )NO] 2+ complex is not toxic to the VSMC in the concentration that it induces maximum relaxation of denuded rat aorta.…”

Section: Development Of Ruthenium-derived No Donor Complexesmentioning

confidence: 99%

Ruthenium Complexes as NO Donors for Vascular Relaxation Induction

Lima

Silva

et al. 2014

Molecules

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Nitric oxide (NO) donors are substances that can release NO. Vascular relaxation induction is among the several functions of NO, and the administration of NO donors is a pharmacological alternative to treat hypertension. This review will focus on the physicochemical description of ruthenium-derived NO donor complexes that release NO via reduction and light stimulation. In particular, we will discuss the complexes synthesized by our research group over the last ten years, and we will focus on the vasodilation and arterial pressure control elicited by these complexes. Soluble guanylyl cyclase (sGC) and potassium channels are the main targets of the NO species released from the inorganic compounds. We will consider the importance of the chemical structure of the ruthenium complexes and their vascular effects.

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Section: Development Of Ruthenium-derived No Donor Complexesmentioning

confidence: 99%

Ruthenium Complexes as NO Donors for Vascular Relaxation Induction

Lima

Silva

et al. 2014

Molecules

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“…Over the past years much attention has been given to nitrosyl-ruthenium complexes and their potential pharmacological uses, especially due to their rapid NO release 8 as well as low level of toxicity 9,[11][12] . Several ruthenium compounds have been synthesized and purified, but so far none has been tested in studies of experimental hypertension induced by blockade of nitric oxide synthase.…”

Section: Discussionmentioning

confidence: 99%

Effects of Rut-bpy (Cis-[Ru(bpy)2(SO3)(NO)]PF 6), a novel nitric oxide donor, in L-NAME-induced hypertension in rats

Campelo¹,

Campelo

Lopes³

et al. 2011

Acta Cir. Bras.

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PURPOSE:To evaluate the effect of Rut-bpy (Cis-[Ru(bpy) 2 (SO 3 )(NO)]PF 6 ), a novel nitric oxide donor in N -nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats. METHODS: Twenty-four male Wistar rats were randomly assigned to four groups (n=6), named according to the treatment applied (G1-Saline, G2-Rut-bpy, G3-L-NAME and G4-L-NAME+Rut-bpy). L-NAME (30 mg/Kg) was injected intraperitoneally 30 minutes before the administration of Rut-bpy (100 mg/Kg). Mean abdominal aorta arterial blood pressure (MAP) was continuously monitored. RESULTS: Mean arterial blood pressure (MAP) in G3 rats rose progressively, reaching 147±16 mmHg compared with 100±19 mm Hg in G1 rats (p<0.05). In G4 rats, treated with L-NAME+Rut-bpy, MAP reached 149+11 mm Hg while in G2 rats, treated with Rut-bpy, MAP values were 106±11 mm Hg. In G1 rats these values decreased progressively reaching 87+14 mm Hg after 30 minutes. An important finding was the maintenance of the MAP throughout the experiment in G2 rats. CONCLUSION: Rut-bpy does not decrease the MAP in L-Name induced hypertensive rats. However, when it is used in anesthetized hypotensive rats a stable blood pressure is obtained. Keywords: Blood Pressure. Nitric Oxide. Ruthenium. Hypertension. Rats. RESUMO OBJETIVO:Avaliar o efeitos do Rut-bpy (Cis-[Ru (bpy) 2 (SO 3 )(NO)] PF 6 ), um novo doador de óxido nítrico, em ratos hipertensos induzidos pelo éster metílico de N-nitro-L-arginina (L-NAME). MÉTODOS: Vinte e quatro ratos Wistar machos foram distribuídos aleatoriamente em quatro grupos (n = 6), nomeados de acordo com o tratamento aplicado (G1-Salina, G2-Rut-bpy, G3-L-NAME e G4-L-NAME+Rut -bpy). L-NAME (30 mg / Kg) foi injetado por via intraperitoneal 30 minutos antes da administração de Rut-bpy (100 mg / kg). A pressão arterial média (PAM) da aorta abdominal foi monitorada continuamente. RESULTADOS: A pressão arterial média (PAM) em ratos do grupo G3 subiu progressivamente, chegando a 147 ±16 mm Hg, em comparação com 100 ±19 mm Hg em ratos do G1 (p <0,05). Em ratos G4, tratados com L-NAME + Rut-bpy, a PAM atingiu 149±11 milímetros de Hg, enquanto no G2 (ratos tratados com Rut bpy) os valores da PAM foram 106 ±11 mm Hg. No G1 esses valores decresceram progressivamente, atingindo 87±14 mm Hg após 30 minutos. Um achado importante foi a manutenção da PAM durante todo o experimento em ratos do grupo G2. CONCLUSÃO: O uso de Rut bpy não diminui a PAM em ratos hipertensos por L-NAME. No entanto, quando ele é usado em ratos anestesiados, hipotensos, uma pressão arterial estável é obtida. Descritores: Pressão Arterial. Óxido Nítrico. Rutênio. Hipertensão. Ratos.

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“…The biological effects of NO depend on the site and source of its production, as well as on its concentration [199]. Excessive production of NO has been implicated in hypotension, inflammation-associated tissue damage, rheumatoid arthritis, and insulin-dependent diabetes mellitus [200][201][202]. On the other hand, diminished NO production is involved in pulmonary hypertension, arteriosclerosis, and reperfusion injury [203].…”

Section: Biological Activitymentioning

confidence: 99%