Targeting heme-oxidized soluble guanylate cyclase with BAY 58-2667 in experimental heart failure
Year: 2007
Type: article
Abstract: Background Signaling via the nitric oxide (NO) – soluble guanylate cyclase (sGC) – cyclic guanosine monophosphate (cGMP) pathway is frequently impaired in cardiovascular disease states providing a rationale for enhancing it pharmacologically. Nitrovasodilators have been used for more than a century to induce vasodilation via the sGC-cGMP pathway; however, the development of tolerance and potentially adverse cGMP-independent actions of nitrovasodilators such as promoting oxidative stress and protein modification are functionally important limitations. BAY 58–2667 is a novel, NO-independent sGC activator which is not associated with the development of tolerance and which preferentially activates oxidized or heme-free sGC, which both are insensitive to endogenous NO and nitrovasodilators [1,2]. In this study we sought to define the cardiorenal actions of BAY 58–2667 as compared to nitroglycerin (NTG) in experimental heart failure (HF). We hypothesized that BAY 58–2667 would potently unload the heart and preserve renal function in a canine model of HF in a manner similar to NTG.
Source: BMC Pharmacology
Institutions: Mayo Clinic, Helios Klinikum Erfurt, Bayer (Germany)
Language: English
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
OpenAlex ID: W2098422956