Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve Pubget Overpricing |
lüll New nitric oxide donors based on ruthenium complexes Lunardi CN; da Silva RS; Bendhack LMBraz J Med Biol Res 2009[Jan]; 42 (1): 87-93Nitric 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.|Animals[MESH]|Aorta/drug effects[MESH]|Calcium Channels/drug effects/physiology[MESH]|Cyclic GMP-Dependent Protein Kinases/*drug effects/metabolism[MESH]|Hypertension, Renal/physiopathology[MESH]|Muscle Relaxation[MESH]|Muscle, Smooth, Vascular/*drug effects/enzymology/physiopathology[MESH]|Nitric Oxide Donors/*pharmacology[MESH]|Nitric Oxide/metabolism[MESH]|Potassium Channels/drug effects/physiology[MESH]|Rats[MESH]|Ruthenium/chemistry/*pharmacology[MESH]|Signal Transduction/drug effects[MESH]|Time Factors[MESH]|Vasodilation/drug effects/physiology[MESH] |