ArticleBritish journal of pharmacology2016
Time-dependent activation of prostacyclin and nitric oxide pathways during continuous i.v. infusion of serelaxin (recombinant human H2 relaxin).
Article in British journal of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- In vitro effect of relaxin in the rat corpus cavernosum under hyperglycemic and normoglycemic conditions.International journal of impotence research · 2024Article
- Time-dependent specific molecular signatures of inflammation and remodelling are associated with trimethylamine-N-oxide (TMAO)-induced endothelial cell dysfunction.Scientific reports · 2023Article
- Gut-Derived Metabolite, Trimethylamine-N-oxide (TMAO) in Cardio-Metabolic Diseases: Detection, Mechanism, and Potential Therapeutics.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Engineered Adipose-Derived Stem Cells Overexpressing RXFP1 via CRISPR Activation Ameliorate Erectile Dysfunction in Diabetic Rats.Antioxidants (Basel, Switzerland) · 2023Article
- Valorization of avocado seeds with antioxidant capacity using pressurized hot water extraction.Scientific reports · 2022Article
- Pressurized Hot Water Extraction of Okra Seeds Reveals Antioxidant, Antidiabetic and Vasoprotective Activities.Plants (Basel, Switzerland) · 2021Article
- Antioxidant and Cytoprotective Effect of Quinoa (Antioxidants (Basel, Switzerland) · 2020Article
- Serelaxin activates eNOS, suppresses inflammation, attenuates developmental delay and improves cognitive functions of neonatal rats after germinal matrix hemorrhage.Scientific reports · 2020Article
- The Novel Small-molecule Annexin-A1 Mimetic, Compound 17b, Elicits Vasoprotective Actions in Streptozotocin-induced Diabetic Mice.International journal of molecular sciences · 2020Article
- Relaxin reduces endothelium-derived vasoconstriction in hypertension: Revealing new therapeutic insights.British journal of pharmacology · 2020Article
- Relaxin 2 fails to lower intraocular pressure and to dilate retinal vessels in rats.International ophthalmology · 2019Article
- Microvascular Dysfunction in Heart Failure With Preserved Ejection Fraction.Frontiers in physiology · 2019Review
- RXFP1 Receptor Activation by Relaxin-2 Induces Vascular Relaxation in MiceFrontiers in physiology · 2018Article
- Relaxin as a Therapeutic Target for the Cardiovascular Complications of Diabetes.Frontiers in pharmacology · 2018Review
- Relaxin Deficiency Leads to Uterine Artery Dysfunction During Pregnancy in Mice.Frontiers in physiology · 2018Article
- Vascular actions of relaxin: nitric oxide and beyond.British journal of pharmacology · 2017Review
- Serelaxin treatment reverses vascular dysfunction and left ventricular hypertrophy in a mouse model of Type 1 diabetes.Scientific reports · 2017Article
- Relaxin-2 in Cardiometabolic Diseases: Mechanisms of Action and Future Perspectives.Frontiers in physiology · 2017Review
- Serelaxin Treatment Reduces Oxidative Stress and Increases Aldehyde Dehydrogenase-2 to Attenuate Nitrate Tolerance.Frontiers in pharmacology · 2017Article
- Time-dependent activation of prostacyclin and nitric oxide pathways during continuous i.v. infusion of serelaxin (recombinant human H2 relaxin).British journal of pharmacology · 2016Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeIn the RELAX-AHF trial, a 48 h i.v. serelaxin infusion reduced systemic vascular resistance in patients with acute heart failure. Consistent with preclinical studies, serelaxin augments endothelial vasodilator function in rat mesenteric arteries. Little is known about the contribution of endothelium-derived relaxing factors after a longer duration of continuous serelaxin treatment. Here we have assessed vascular reactivity and mechanistic pathways in mesenteric arteries and veins and the aorta after 48 or 72 h continuous i.v. infusion of serelaxin. EXPERIMENTAL APPROACH: Male rats were infused with either placebo or serelaxin (13.3 μg·kg(-1) ·h(-1) ) via the jugular vein using osmotic minipumps. Vascular function was assessed using wire myography. Changes in gene and protein expression and 6-keto PGF1α levels were determined by quantitative PCR, Western blot and ELISA respectively. KEY
resultsContinuous i.v. serelaxin infusion augmented endothelium-dependent relaxation in arteries (mesenteric and aorta) but not in mesenteric veins. In mesenteric arteries, 48 h i.v. serelaxin infusion increased basal NOS activity, associated with increased endothelial NOS (eNOS) expression. Interestingly, phosphorylated-eNOS(Ser1177) , eNOS and basal NOS activity were reduced in mesenteric arteries following 72 h serelaxin treatment. At 72 h, serelaxin treatment improved bradykinin-mediated relaxation through COX2-derived PGI2 production. CONCLUSIONS AND IMPLICATIONS: Continuous i.v. serelaxin infusion enhanced endothelial vasodilator function in arteries but not in veins. The underlying mediator at 48 h was NO but there was a transition to PGI2 by 72 h. Activation of the PGI2 -dependent pathway is key to the prolonged vascular response to serelaxin treatment.
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