Key result
Nitrosyl ruthenium complexes act as nitric oxide delivery agents to induce vascular smooth muscle relaxation, though this effect is impaired in hypertensive models due to oxidative stress.
Nitrosyl ruthenium complexes represent a promising new class of NO donors that effectively induce vascular relaxation, though their efficacy is blunted in hypertensive states characterized by oxidative stress.
No immediate clinical role for nitrosyl ruthenium complexes; leaves open their development as NO donors pending targeted research.
Nitric oxide (NO) donors produce NO-related activity when applied to biological systems. Among its diverse functions, NO has been implicated in vascular smooth muscle relaxation. Despite the great importance of NO in biological systems, its pharmacological and physiological studies have been limited due to its high reactivity and short half-life. In this review we will focus on our recent investigations of nitrosyl ruthenium complexes as NO-delivery agents and their effects on vascular smooth muscle cell relaxation. The high affinity of ruthenium for NO is a marked feature of its chemistry. The main signaling pathway responsible for the vascular relaxation induced by NO involves the activation of soluble guanylyl-cyclase, with subsequent accumulation of cGMP and activation of cGMP-dependent protein kinase. This in turn can activate several proteins such as K+ channels as well as induce vasodilatation by a decrease in cytosolic Ca2+. Oxidative stress and associated oxidative damage are mediators of vascular damage in several cardiovascular diseases, including hypertension. The increased production of the superoxide anion (O2-) by the vascular wall has been observed in different animal models of hypertension. Vascular relaxation to the endogenous NO-related response or to NO released from NO deliverers is impaired in vessels from renal hypertensive (2K-1C) rats. A growing amount of evidence supports the possibility that increased NO inactivation by excess O2- may account for the decreased NO bioavailability and vascular dysfunction in hypertension.
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Lunardi et al. (2009) conducted a review in Hypertension. Nitrosyl ruthenium complexes was evaluated. Nitrosyl ruthenium complexes act as nitric oxide delivery agents to induce vascular smooth muscle relaxation, though this effect is impaired in hypertensive models due to oxidative stress.
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