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• W2172161724 abstract "Background: Soluble guanylate cyclase (sGC) is a heterodimeric enzyme with a prosthetic heme group. It can be regarded as a key enzyme in cardiovascular regulation, as it is the target of nitric oxide(NO) and a producer of the second messenger cyclic guanosine monophosphate (cGMP). Recently, we reported the cardiorenal actions of the NO-independent, but heme-dependent direct sGC stimulator BAY 41-2272 in experimental congestive heart failure (CHF). It acted primarily as an arterial vasodilator, and, unlike nitroglycerin, did not decrease right atrial pressure (Circulation, 2003). The new BAY 58-2667, which is orally available and devoid of tolerance development with chronic administration, directly stimulates sGC in a heme-independent manner. Here we report for the first time the cardiorenal actions of the new NO- and heme-independent direct sGC activator BAY 58-2667 in CHF. Methods: CHF was induced in seven male mongrel dogs by rapid right ventricular pacing at 240 beats per minute for ten days. In an acute study hemodynamic, renal, and humoral parameters were measured in clearances at baseline and with two intravenous doses of BAY 58-2667 (0.1 and 0.3 microgram/kg/min, respectively). Data are expressed as mean±SEM. ∗indicates a p-value <0.05. Results: BAY 58-2667 reduced mean arterial pressure (from 97±6 to 82±5∗ and 68±4∗ mmHg), right atrial pressure (7±1 to 5±1∗ and 3±1∗ mmHg), pulmonary artery pressure (24±1 to 20±1∗ and 17±1∗ mmHg), pulmonary capillary wedge pressure (19±1 to 15±1∗ and 12±2∗ mmHg), systemic vascular resistance (39±4∗ to 33±4∗ and 23±3∗ mmHg/L/min), and renal vascular resistance (578±101 to 393±49 and 306±32∗ mmHg/L/min). In contrast, cardiac output (2.4±0.3 to 2.7±0.4 and 3.1±0.4∗ L/min) and renal blood flow (165±15 to 201±16 and 218±17∗ mL/min) increased. Urinary flow, glomerular filtration rate, plasma renin activity, angiotensin II, and aldosterone remained unchanged despite the decrease in mean arterial pressure. Atrial and B-type natriuretic peptide decreased with the higher dose. Conclusion: Intravenous administration of BAY 58-2667, a novel heme-independent direct soluble guanylate cyclase activator, in experimental CHF potently unloads the heart and results in systemic and renal vasodilation. This occurred with maintenance of renal function and without further activation of the renin-angiotensin-aldosterone system. Both ANP and BNP served as biomarkers for the cardiac unloading actions. Given that BAY 58-2667 is not associated with tolerance development and stimulates sGC without the potential adverse cGMP-independent effects of NO, BAY 58-2667 may be a novel, beneficial treatment for CHF." @default.
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• W2172161724 date "2003-10-01" @default.
• W2172161724 modified "2023-10-16" @default.
• W2172161724 title "Cardiorenal actions of the new heme-independent direct soluble guanylate cyclase activator BAY 58-2667 in experimental congestive heart failure" @default.
• W2172161724 doi "https://doi.org/10.1016/s1071-9164(03)00214-8" @default.
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