ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
Cinaciguat, a soluble guanylate cyclase activator, causes potent and sustained pulmonary vasodilation in the ovine fetus.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 43 citations in OpenAlex.
- Pharmacokinetics and Lung Deposition After Administration of Inhaled Mosliciguat (BAY 1237592): Results from Randomized Phase I Studies in Healthy Men.Clinical pharmacokinetics · 2025Trial
- Inhaled mosliciguat (BAY 1237592): targeting pulmonary vasculature via activating apo-sGC.Respiratory research · 2022Article
- Pulmonary vasodilator strategies in neonates with acute hypoxemic respiratory failure and pulmonary hypertension.Seminars in fetal & neonatal medicine · 2022Review
- Novel use of riociguat in infants with severe pulmonary arterial hypertension unable to wean from inhaled nitric oxide.Frontiers in pediatrics · 2022Article
- Cinaciguat (BAY-582667) Modifies Cardiopulmonary and Systemic Circulation in Chronically Hypoxic and Pulmonary Hypertensive Neonatal Lambs in the Alto Andino.Frontiers in physiology · 2022Article
- Redox Switches Controlling Nitric Oxide Signaling in the Resistance Vasculature and Implications for Blood Pressure Regulation: Mid-Career Award for Research Excellence 2020.Hypertension (Dallas, Tex. : 1979) · 2021Review
- A new paradigm for gaseous ligand selectivity of hemoproteins highlighted by soluble guanylate cyclase.Journal of inorganic biochemistry · 2021Review
- Therapies that enhance pulmonary vascular NO-signaling in the neonate.Nitric oxide : biology and chemistry · 2020Review
- Study of the Effect of Treatment With Atrial Natriuretic Peptide (ANP) and Cinaciguat in Chronic Hypoxic Neonatal Lambs on Residual Strain and Microstructure of the Arteries.Frontiers in bioengineering and biotechnology · 2020Article
- Persistent Pulmonary Hypertension of the Newborn: Pathophysiological Mechanisms and Novel Therapeutic Approaches.Frontiers in pediatrics · 2020Review
- Redox regulation of soluble guanylyl cyclase.Nitric oxide : biology and chemistry · 2018Review
- Irreversible Activation and Stabilization of Soluble Guanylate Cyclase by the Protoporphyrin IX Mimetic Cinaciguat.Molecular pharmacology · 2018Article
- Pharmacologic strategies in neonatal pulmonary hypertension other than nitric oxide.Seminars in perinatology · 2016Review
- Role of reactive oxygen species in neonatal pulmonary vascular disease.Antioxidants & redox signaling · 2014Review
- The soluble guanylyl cyclase activator BAY 60-2770 potently relaxes the pulmonary artery on congenital diaphragmatic hernia rabbit model.Pediatric surgery international · 2014Article
- Vasodilator responses to acetylcholine are not mediated by the activation of soluble guanylate cyclase or TRPV4 channels in the rat.American journal of physiology. Heart and circulatory physiology · 2014Article
- The soluble guanylyl cyclase activator bay 58-2667 selectively limits cardiomyocyte hypertrophy.PloS one · 2012Article
- Cinaciguat, a soluble guanylate cyclase activator, augments cGMP after oxidative stress and causes pulmonary vasodilation in neonatal pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- New perspectives for the treatment of pulmonary hypertension.British journal of pharmacology · 2011Review
- Pulmonary and systemic vasodilator responses to the soluble guanylyl cyclase activator, BAY 60-2770, are not dependent on endogenous nitric oxide or reduced heme.American journal of physiology. Heart and circulatory physiology · 2011Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Impaired nitric oxide-cGMP signaling contributes to severe pulmonary hypertension after birth, which may in part be due to decreased soluble guanylate cyclase (sGC) activity. Cinaciguat (BAY 58-2667) is a novel sGC activator that causes vasodilation, even in the presence of oxidized heme or heme-free sGC, but its hemodynamic effects have not been studied in the perinatal lung. We performed surgery on eight fetal (126 +/- 2 days gestation) lambs (full term = 147 days) and placed catheters in the main pulmonary artery, aorta, and left atrium to measure pressures. An ultrasonic flow transducer was placed on the left pulmonary artery to measure blood flow, and a catheter was placed in the left pulmonary artery for drug infusion. Cinaciguat (0.1-100 microg over 10 min) caused dose-related increases in pulmonary blood flow greater than fourfold above baseline and reduced pulmonary vascular resistance by 80%. Treatment with 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), an sGC-oxidizing inhibitor, enhanced cinaciguat-induced pulmonary vasodilation by >120%. The pulmonary vasodilator effect of cinaciguat was prolonged, decreasing pulmonary vascular resistance for >1.5 h after brief infusion. In vitro stimulation of ovine fetal pulmonary artery smooth muscle cells with cinaciguat after ODQ treatment resulted in a 14-fold increase in cGMP compared with non-ODQ-treated cells. We conclude that cinaciguat causes potent and sustained fetal pulmonary vasodilation that is augmented in the presence of oxidized sGC and speculate that cinaciguat may have therapeutic potential for severe neonatal pulmonary hypertension.
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Registered trials
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