Relaxin Inhibits Spontaneous and Prostaglandin-Driven Myometrial Activity in Anaesthetized Rats

Porter, D. G.; Downing, Sandra J.; Bradshaw, Jane M. C.

doi:10.1677/joe.0.0830183

Cited by 60 publications

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“…The ability of rat relaxin to inhibit myometrial activity in vivo and in vitro, and to soften the uterine cervix is consistent with the reports of McMurtry, Kwok & Bryant-Greenwood (1978), Mercado-Simmen, Bryant-Greenwood & Greenwood (1980) and Cheah & Sherwood (1980) that these tissues possess receptors for relaxin as evidenced by their binding of 12SI-labelled relaxin. These findings support the suggestion (Porter, 1979b) (Porter, Downing & Bradshaw, 1979). The finding that the rate of rise of intrauterine pressure was significantly elevated after treatment suggests that relaxin improves myometrial co-ordination.…”

Section: Discussionsupporting

confidence: 87%

Demonstration of some of the physiological properties of rat relaxin

Bradshaw¹,

Downing²,

Moffatt³

et al. 1981

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Summary. Relaxin was extracted from the ovaries of pregnant rats. Material possessing uterine relaxing activity in vitro was eluted in three peaks from Sephadex G.50 columns. The 'G3 peak' material eluting in a position comparable to that of porcine relaxin inhibited myometrial activity of rats in vivo, improved the rate of rise of pressure of intrauterine pressure cycles in vivo, and, when administered to rats following progesterone and oestrogen priming, increased the distensibility of the cervix in vitro. This material also stimulated inter-pubic ligament formation in the mouse. This rat relaxin material therefore exhibits biological actions in the rat similar to those previously assigned to porcine relaxin.

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Section: Discussionsupporting

confidence: 87%

Demonstration of some of the physiological properties of rat relaxin

Bradshaw¹,

Downing²,

Moffatt³

et al. 1981

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“…In addition to its classical actions on cervical ripening, uterine contraction, and pubic symphysis elongation (1,2), relaxin has been suggested to participate in the regulation of blood pressure (3)(4)(5)(6)(7)(8) and neuropeptide release, notably oxytocin and vasopressin (9)(10)(11)(12)(13). However, the results from these studies were conflicting, and the site of action of relaxin was undetermined.…”

mentioning

confidence: 99%

Relaxin binding in the rat heart atrium.

Osheroff¹,

Cronin²,

Lofgren³

1992

Proc. Natl. Acad. Sci. U.S.A.

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Relaxin is a member of the insulin family of polypeptides that is best known as a reproductive hormone. In an effort to elucidate the mechanism of action of relaxin we previously localized the specific binding sites of a 32P-labeled relaxin in the rat uterus and brain. These studies suggested that, in addition to its classical role in pregnancy, relaxin might have other physiological functions. In the present paper we describe the specific and high-afminity binding of relaxin to the cardiac atrium of both male and female rats. The relaxin binding could not be displaced by peptides belonging to the same family [insulin, insulin-like growth factor I (IGF-I)] or by peptides that were identified in the atrium or were known to have cardiovascular functions (atrial natriuretic peptide, angiotensin II). The dissociation constant for relaxin in the atrium was estimated to be 1.4 nM, which was similar to that found in the uterus (1.3 nM) and the brain (1.4 nM). In view of the close association of relaxin with reproduction, an experiment was also performed to compare the relaxin binding in the uterus and heart after gonadectomy and sex steroid treatment. It was found that the relaxin binding in the rat uterus was diminished by 53% overall following ovariectomy but was restored to 90% of normal levels when treated with estrogen (but not with testosterone). In contrast, the relaxin binding in the rat heart was not affected by castration or sex steroid treatment. We conclude that specific and high-affinity relaxin receptors exist in the atrium of both the male and female rat heart and that these are regulated differently than the relaxin receptors in the uterus.Relaxin is structurally related to insulin and insulin-like growth factors and is best known as a pregnancy-associated hormone (1, 2). In addition to its classical actions on cervical ripening, uterine contraction, and pubic symphysis elongation (1, 2), relaxin has been suggested to participate in the regulation of blood pressure (3-8) and neuropeptide release, notably oxytocin and vasopressin (9-13). However, the results from these studies were conflicting, and the site of action of relaxin was undetermined. Biochemical support for these hypotheses was provided when it was shown that, in addition to the uterus and cervix (14), relaxin bound with specificity and high affinity (Kd 1 nM) to several sites in the male and female rat brain (15). Some of these sites, in particular two of the circumventricular organs (subfornical organ and organum vasculosum of the lamina terminalis) and the magnocellular hypothalamic nuclei (paraventricular and supraoptic nucleus) are known to be involved in the control of blood pressure, fluid balance, and the release of neuropeptides. To further investigate the mechanism of action of relaxin, we continued the search for relaxin target tissues and were surprised to observe the specific and high-affinity binding of relaxin to the atrium of the rat heart. We also show that the atrial binding is regulated differently than the uterus. ...

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“…Miller et al (4) first reported that injection of an extract of pregnant sow ovary caused a transient fall in blood pressure when injected into anaesthetized dogs. In contrast, injection of up to 50 pg purified porcine relaxin in anaesthetized rats did not affect blood pressure (5). Preliminary experiments reported by Jones and Summerlee (6) indicated that acute iv injections of a standard dose of relaxin caused a rise in blood pressure and the release of vasopressin.…”

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Mechanism of the Haemotensive Action of Porcine Relaxin in Anaesthetized Rats

Parry

Poterski

Summerlee

et al. 1990

J Neuroendocrinology

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Experiments were done to examine the pressor effect of iv porcine relaxin in anaesthetized rats. Acute injections of relaxin caused consistent and sustained rises in systemic blood pressure that were dose-dependent within the physiological range. Pretreatment of rats with a specific vasopressin ( V l ) receptor antagonist, but not an a-adrenoreceptor antagonist, substantially reduced the pressor effect of relaxin. After the vasopressin receptor antagonist, small rises in blood pressure occurred after a longer latent period, compared with the responses in intact animals. The data clearly indicate that acute injections of relaxin cause a pressor response that is predominantly affected via the release of vasopressin. The possible sources of the persistent hypertensive component are discussed and it is suggested that relaxin might act through the central angiotensinergic systems to release vasopressin and cause a pressor response.Plasma relaxin concentrations show marked changes during pregnancy in many species (1). In the rat, the levels of relaxin become detectable from about Day 10 of gestation and rise progressively to reach levels of approximately 100 ng/ml by Day 19. Immediately before birth there is a further, substantial rise in plasma relaxin, followed by a precipitous fall (2). Relaxin has well established roles in the periphery preparing the uterus, cervix and ligaments of the pelvic girdle for birth (1). It also appears to have a central role controlling the release of oxytocin and may be important for determining the timing of birth (3). However, relaxin may also modulate the release of vasopressin, and thereby affect blood pressure. Reports in the literature concerning the effects of relaxin on blood pressure are conflicting and contradictory. Miller et al. (4) first reported that injection of an extract of pregnant sow ovary caused a transient fall in blood pressure when injected into anaesthetized dogs. In contrast, injection of up to 50 pg purified porcine relaxin in anaesthetized rats did not affect blood pressure (5). Preliminary experiments reported by Jones and Summerlee (6) indicated that acute iv injections of a standard dose of relaxin caused a rise in blood pressure and the release of vasopressin. These latter experiments are consistent with the centrally mediated pressor effect of relaxin injected into the third ventricle that is also accompanied by a release of vasopressin (7). The purpose of the present experiments was a thorough reexamination of the possible pressor effects of iv relaxin in anaesthetized rats, to clarify the extent of the pressor response, whether or not it was dose-dependent and to elucidate the possible mechanisms of action. ResultsPressor effects of iv injections of relaxin Acute iv injections of porcine relaxin caused significant (P < 0.01) and sustained increases in blood pressure, compared with control injections of either non-relaxin protein or saline, in anaesthetized female rats (Fig. 1). These increases were dose-dependent within the range 1.25 pg to 10...

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Relaxin Inhibits Spontaneous and Prostaglandin-Driven Myometrial Activity in Anaesthetized Rats

Cited by 60 publications

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Demonstration of some of the physiological properties of rat relaxin

Demonstration of some of the physiological properties of rat relaxin

Relaxin binding in the rat heart atrium.

Mechanism of the Haemotensive Action of Porcine Relaxin in Anaesthetized Rats

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