Relaxin has beneficial effects on liver lipidome and metabolic enzymes.

Relaxin is an insulin-like hormone with pleiotropic protective effects in several organs, including the liver. We aimed to characterize its role in the control of hepatic metabolism in healthy rats. Sprague-Dawley rats were treated with human recombinant relaxin-2 for 2 weeks.

Serelaxin (recombinant human relaxin-2) treatment affects the endogenous synthesis of long chain poly-unsaturated fatty acids and induces substantial alterations of lipidome and metabolome profiles in rat cardiac tissue.

Background And Purpose: Recombinant human relaxin-2, serelaxin, is being proved as a novel drug with therapeutic efficacy in some cardiovascular diseases, especially heart failure, a disease whose physiopathology and course are firmly correlated with important alterations in cardiac metabolism. The aim of our present work was to investigate changes in the cardiac metabolome following relaxin-2 treatment.

Experimental Approach: Sprague-Dawley rats were treated with human recombinant relaxin-2 using osmotic minipumps at a dose of 0.

Efficacy of relaxin on functional recovery of post stroke patients.

Background: Relaxin is a peptide hormone that exerts specific effects on cardiovascular system and human brain, leading to the hypothesis that this hormone may play a protective role against CVD and integration and modulation of behavioral activation. We aimed to demonstrate the efficacy of Relaxin on functional recovery of post-stroke patients.

Methods: Patients admitted within a Rehabilitation Unit suffering from stroke have been evaluated.

Efficacy and safety of oral porcine relaxin (pRLX) in adjunct to physical exercise in the treatment of peripheral arterial disease (PAD).

Introduction: PAD medical therapy has a number of limitations. RLX showed promises in experimental model mainly through NO release. Our study is the first to evaluate the efficacy and safety of RLX in PAD.

Relaxin as a cardiovascular drug: a promise kept.

Relaxin (RLX), formerly known for its effects on reproduction and pregnancy, has been later shown to be a pleiotropic hormone, capable of also targeting numerous non-reproductive organs of the cardiovascular, nervous, respiratory, tegumental, excretory and digestive systems. Most of these effects have been studied in animal models, but there is compelling evidence that RLX also acts in humans. In more recent years, human luteal-type (H2) RLX synthesised by recombinant DNA technology has been investigated in clinical trials, mostly oriented to assess its therapeutic potential in cardiovascular disease.

Clinical profile of relaxin, a possible new drug for human use.

Relaxin (RLX) belongs to the relaxin hormone super-family, which in humans includes 3 RLX molecules and 4 insulin-like peptides. Of these, luteal RLX is the main circulating form in animals and man. RLX, formerly known for its effects on reproduction and pregnancy, has been demonstrated to act on numerous other targets, including the cardiovascular, central and peripheral nervous, respiratory, tegument, excretory and digestive systems.

A novel, simple bioactivity assay for relaxin based on inhibition of platelet aggregation.

In humans, the relaxin hormone family includes H1, H2 and H3 isoforms and insulin-like peptides 3 to 6. The ever-increasing interest in relaxin as potential new drug requires reliable methods to compare bioactivity of different relaxins. The existing bioassays include in vivo or ex vivo methods evaluating the organ-specific responses to relaxin and in vitro methods based on measurement of cAMP increase in relaxin receptor-bearing cells.

Relaxin as a cardiovascular hormone: physiology, pathophysiology and therapeutic promises.

Relaxin is a hormone belonging to the so-called relaxin superfamily, which also includes insulin-like peptides. Relaxin is best known for its effects on the female reproductive system, which primarily include lengthening of the pubic symphysis and softening of the tissues of the birth canal, stimulating mammary and endometrial development, and maintenance of myometrial quiescence. In recent years, evidence has been accumulating that relaxin can have multiple and diverse effects on both reproductive and nonreproductive organs, tissues and cells, thus acting as a sort of 'manager' hormone to optimize the many physiological changes taking place during pregnancy.

Novel drug development opportunity for relaxin in acute myocardial infarction: evidences from a swine model.

The hormone relaxin has been shown to cause coronary vasodilation and to prevent ischemia/reperfusion-induced cardiac injury in rodents. This study provides evidence that relaxin, used as an adjunctive drug to coronary reperfusion, reduces the functional, biochemical, and histopathological signs of myocardial injury in an in vivo swine model of heart ischemia/reperfusion, currently used to test cardiotropic drugs for myocardial infarction. Human recombinant relaxin, given at reperfusion at doses of 1.

Human recombinant relaxin reduces heart injury and improves ventricular performance in a swine model of acute myocardial infarction.

This study shows that relaxin can be effective in the treatment of acute myocardial infarction. In a swine model of heart ischemia-reperfusion currently used to test cardiotropic drugs because of its similarities with human myocardial infarction, human recombinant relaxin (2.5 and 5 microg/kg body weight), given at reperfusion after a 30-min ischemia, markedly reduced the main serum markers of myocardial damage (myoglobin, CK-MB, and troponin T) and the metabolic and histopathologic parameters of myocardial inflammation and cardiomyocyte injury, resulting in overall improvement of ventricular performance (increased cardiac index) compared to the controls.

Basic progress and future therapeutic perspectives of relaxin in ischemic heart disease.

Relaxin has been validated as a cardiotropic hormone, being produced by the heart and acting on specific heart receptors. Evidence is accumulating that it could hamper the pathophysiologic mechanisms of ischemic heart disease. Time is ripe to study relaxin as a cardiotropic drug, as recombinant human relaxin (hrRLX) is now available and previous clinical trials have shown a virtual lack of toxicity and adverse side effects, even at high doses.

Influence of relaxin on the neurally induced relaxant responses of the mouse gastric fundus.

The peptide hormone relaxin has been reported to depress the amplitude of contractile responses in the mouse gastric fundus by upregulating nitric oxide (NO) biosynthesis at the neural level. In the present study, we investigated whether relaxin also influenced nonadrenergic, noncholinergic (NANC) gastric relaxant responses in mice. Female mice in proestrus or estrus were treated for 18 h with relaxin (1 microg s.

Depression by relaxin of neurally induced contractile responses in the mouse gastric fundus.

The peptide hormone relaxin, which attains high circulating levels during pregnancy, has been shown to depress small-bowel motility through a nitric oxide (NO)-mediated mechanism. In the present study we investigated whether relaxin also influences gastric contractile responses in mice. Female mice in proestrus or estrus were treated for 18 h with relaxin (1 microg s.

Inhibitory effects of relaxin on human basophils activated by stimulation of the Fc epsilon receptor. The role of nitric oxide.

This study investigates whether relaxin (RLX), a hormone previously shown to inhibit mast cell function and to stimulate endogenous nitric oxide (NO) biosynthesis, counteracts the activation of isolated human basophils stimulated with anti-IgE or phorbol ester, and, if so, whether NO is involved. RLX reduced dose-dependently the expression of the activation marker CD63, the release of histamine and the rise of intracellular Ca2+ levels which triggers granule release by stimulated basophils. RLX also blunts the ultrastructural signs of anaphylactic granule release.

Relaxin depresses small bowel motility through a nitric oxide-mediated mechanism. Studies in mice.

Gastrointestinal motility is reduced and the incidence of functional gastrointestinal disorders is increased in pregnancy, possibly due to hormonal influences. This study aims to clarify whether the hormone relaxin, which attains high circulating levels during pregnancy and has a nitric oxide-mediated relaxant action on vascular and uterine smooth muscle, also reduces bowel motility and, if it does, whether nitric oxide is involved. Female mice in proestrous or estrous were treated for 18 h with relaxin (1 microg s.

Relaxin up-regulates inducible nitric oxide synthase expression and nitric oxide generation in rat coronary endothelial cells.

Relaxin (RLX) is a reproductive hormone with vasodilatatory properties on several organs, including the heart. RLX-induced vasodilatation appears to depend on the stimulation of endogenous NO production. Here, we investigate whether RLX acts on rat coronary endothelial (RCE) cells in vitro by inducing changes of NO generation and, if so, to clarify the possible mechanism of action.