Target Tissues for Relaxin in the Rat: Tissue Distribution of Injected<sup>125</sup>I-Labeled Relaxin and Tissue Changes in Adenosine 3′, 5′-Monophosphate Levels after<i>in Vitro</i>Relaxin Incubation*

Cheah, Swee Hung; Sherwood, O. D.

doi:10.1210/endo-106-4-1203

Cited by 65 publications

(40 citation statements)

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“…This con®rms earlier studies using [ 32 P]-h2Rlx (B33) (Oshero & Phillips, 1991;Oshero et al, 1992) or [ 125 I]-labelled porcine relaxin (Cheah & Sherwood, 1980;Yang et al, 1992) but only one study quantitatively measured the density of binding sites . One published study showed that saturation of [ 125 I]-porcine relaxin binding was biphasic in rat uterus (Mercado-Simmen et al, 1980).…”

Section: Discussionsupporting

confidence: 88%

Quantitative autoradiographic studies of relaxin binding in rat atria, uterus and cerebral cortex: characterization and effects of oestrogen treatment

Tan

Wade

Tregear

et al. 1999

British J Pharmacology

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1 The binding characteristics of the relaxin receptor in rat atria, uterus and cortex were studied using a [ 33 P]-labelled human gene 2 relaxin (B33) and quantitative receptor autoradiography. 2 The binding kinetics of [ 33 P]-human gene 2 relaxin (B33) were investigated in slide-mounted rat atrial sections. The binding achieved equilibrium after 60 min incubation at room temperature (23+18C) and dissociated slowly. The association and dissociation rate constants were 4.31+0.34610 8 M 71 min 71 and 1.55+0.38610 73 min 71 respectively. Thus, the kinetic dissociation constant was 3.46+0.59 pM. 3 Binding was saturable to a single population of non-interacting sites throughout atria, in uterine myometrium and the 5th layer of cerebral cortex. The binding a nities (pK D ) of [ 33 P]-human gene 2 relaxin (B33) were 8.92+0.09 in atrial myocardium and 8.79+0.04 in cerebral cortex of male rats, and 8.79+0.10 in uterine myometrium. Receptor densities in the cerebral cortex and atria were higher than in uterine myometrium, indicating that relaxin also has important roles in nonreproductive tissues. 4 In male rats, treatment with 17b-oestradiol (20 mg in 0.1 ml sesame oil s.c., 18 ± 24 h) signi®cantly decreased the density of relaxin receptors in atria and cerebral cortex. Identical treatment in female rats had no signi®cant e ect in atria and cerebral cortex, but it signi®cantly increased the density of relaxin receptors in uterine myometrium. 5 Relaxin binding was competitively displaced by porcine and rat native relaxins. Porcine native relaxin binds to the relaxin receptor in male rat atria (8.90+0.02), and cerebral cortex (8.90+0.03) and uterine myometrium (8.89+0.03) with a nities not signi®cantly di erent from human gene 2 (B33) relaxin. Nevertheless, rat relaxin binds to the receptors with a nities (8.35+0.09 in atria, 8.22+0.07 in cerebral cortex and 8.48+0.06 in uterine myometrium) signi®cantly less than human gene 2 (B33) and porcine relaxins. 6 Quantitative receptor autoradiography is the method of choice for measurement of a nities and densities of relaxin receptor in atria, uterine myometrium and cerebral cortex. High densities were found in all these tissues. 17b-Oestradiol treatment produced complex e ects where it increased the densities of relaxin receptors in uterus but decreased those in atria and cerebral cortex of the male rats, and had no e ect on the atria and cerebral cortex of the female rats.

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Section: Discussionsupporting

confidence: 88%

Quantitative autoradiographic studies of relaxin binding in rat atria, uterus and cerebral cortex: characterization and effects of oestrogen treatment

Tan

Wade

Tregear

et al. 1999

British J Pharmacology

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“…Specific binding was not displaced by insulin or insulin-like growth factor I or II. Relaxinbinding sites were identified in the uterus of rat (McMurtry et al, 1978;Cheah and Sherwood, 1980;Mercado-Simmen et al, 1980), mouse (McMurtry et al, 1978;Yang et al, 1992) and pig (Mercado et al, 1982); the pubic symphysis of mouse (McMurtry et al, 1978;Yang et al, 1992) and guinea pig (McMurtry et al, 1978); the cervix of pig (Mercado et al, 1982), rat (Weiss and Bryant, 1982) and guinea pig (McMurtry et al, 1978); the rat mammary gland (McMurtry et al, 1978); human fetal membranes (Koay et al, 1986); and fibroblasts from the mouse pubic symphysis and human skin (McMurtry et al, 1980). H2 relaxin contains a tyrosine residue that can be labeled by conventional chloramine-T iodination (Tang and Chegini, 1995).…”

Section: A Relaxin Bindingmentioning

confidence: 99%

“…Early studies of the biochemical effects of relaxin demonstrated an association with increases in cAMP in target tissues (Braddon, 1978;Cheah and Sherwood, 1980;Sanborn et al, 1980). Increased intracellular cAMP was observed in mouse pubic symphysis (Braddon, 1978), in rat uterus (Cheah and Sherwood, 1980;Judson et al, 1980;Sanborn et al, 1980), and in cultures of rat (Hsu et al, 1985) and rhesus monkey myometrium (Kramer et al, 1990), human endometrium (Chen et al, 1988;Fei et al, 1990), rat anterior pituitary cell (Cronin et al, 1987), and human THP-1 monocytes (Parsell et al, 1996).…”

Section: A Signaling In Response To Relaxinmentioning

confidence: 99%

International Union of Pharmacology LVII: Recommendations for the Nomenclature of Receptors for Relaxin Family Peptides

Bathgate

Ivell²,

Sanborn³

et al. 2006

Pharmacol Rev

294

256

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“…Specific relaxin binding sites exist for relaxin not only in reproductive tissues (26,(69)(70)(71)(72) but also in the heart and brain (27,28). Some of the most intense relaxin binding, indicated by computerized densitometry, occurs in a number of hypothalamic and forebrain nuclei, including the supraoptic and paraventricular nuclei, the organum vasculosum of the lamina terminalis and the subfornical organ.…”

Section: Relaxin Binding Sites In the Brainmentioning

confidence: 99%

The Emerging Concept of Relaxn as a Centrally Actng Peptide Hormone with Hemodynamic Actions

Geddes

Summerlee

1995

J Neuroendocrinology

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The novel finding that relaxin has an action on the brain was first published in 1984. Since then, it has been shown that exogenous relaxin affects the release of a number of hypothalamo-pituitary hormones and has a robust pressor action. In this paper, we review the accumulating evidence that relaxin affects the release of oxytocin and vasopressin by an action at the level of the brain. The potential mechanisms of this central action are discussed and the evidence presented for the interaction between relaxin and the forebrain angiotensin-ll system. Furthermore, we articulate the possible physiological influences of relaxin on the changes in cardiovascular function that occur during pregnancy.F. L. Hisaw ( I ) discovered an ovarian substance that caused relaxation of the pelvic ligament of a variety of species in 1926 but it was not until 1930 that the first crude extract of the substance was obtained and named relaxin (2). Initial work focused on the role of relaxin on the birth canal and it was not until 1957 that an effect on the cardiovascular system was first reported (3). Miller and colleagues (3) showed that an extract of ovary caused a short hypotensive episode in dogs and suggested that relaxin had a direct action on peripheral blood vessels. Since that time. a number of hemodynamic actions of relaxin have been described (4, 5). The balance of the data, however, suggests that relaxin is hypertensive and exerts this effect through an action at the level of the brain (6-9) and on the heart (10, 11). RelaxinRelaxin is a peptide hormone produced primarily by the corpus luteum, placenta, uterus and possibly brain. It is present in detectable quantities in the peripheral circulation only during pregnancy. There are considerable species differences in the site and pattern of release of the hormone, hormone structure, and the putative role the hormone plays in the preparturient period. These differences have been extensively reviewed by Sherwood (4). Most research into the physiological actions of relaxin has been carried out using porcine relaxin obtained by the method described by Sherwood and O'Byrne (12). The classic actions of relaxin in pregnancy include softening of the cervix (13), separation of the pelvic symphysis (14). and maintenance of myornetrial quiescence towards the end of pregnancy ( 15).In the rat, relaxin is produced almost entirely within the corpora lutea of pregnancy (16) although there is some evidence that the hormone may also be produced by the endometrium (17). Levels of hormone are below the limit of detectability, by radioimmunoassay. during the first 7/12 days of pregnancy and start to increase from day 7 onwards. The levels increase steadily until day 16 when they begin to plateau. In the 48 h before birth, in association with the collapse of the corpora lutea, relaxin levels show a sharp peak then fall to low levels before birth starts (18). Sherwood et al. (18) also reported that there were peaks of relaxin in parturition. Although these data have not been confirmed by ...

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Target Tissues for Relaxin in the Rat: Tissue Distribution of Injected¹²⁵I-Labeled Relaxin and Tissue Changes in Adenosine 3′, 5′-Monophosphate Levels afterin VitroRelaxin Incubation*

Cited by 65 publications

References 0 publications

Quantitative autoradiographic studies of relaxin binding in rat atria, uterus and cerebral cortex: characterization and effects of oestrogen treatment

Quantitative autoradiographic studies of relaxin binding in rat atria, uterus and cerebral cortex: characterization and effects of oestrogen treatment

International Union of Pharmacology LVII: Recommendations for the Nomenclature of Receptors for Relaxin Family Peptides

The Emerging Concept of Relaxn as a Centrally Actng Peptide Hormone with Hemodynamic Actions

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Target Tissues for Relaxin in the Rat: Tissue Distribution of Injected125I-Labeled Relaxin and Tissue Changes in Adenosine 3′, 5′-Monophosphate Levels afterin VitroRelaxin Incubation*

Cited by 65 publications

References 0 publications

Quantitative autoradiographic studies of relaxin binding in rat atria, uterus and cerebral cortex: characterization and effects of oestrogen treatment

Quantitative autoradiographic studies of relaxin binding in rat atria, uterus and cerebral cortex: characterization and effects of oestrogen treatment

International Union of Pharmacology LVII: Recommendations for the Nomenclature of Receptors for Relaxin Family Peptides

The Emerging Concept of Relaxn as a Centrally Actng Peptide Hormone with Hemodynamic Actions

Contact Info

Product

Resources

About

Target Tissues for Relaxin in the Rat: Tissue Distribution of Injected¹²⁵I-Labeled Relaxin and Tissue Changes in Adenosine 3′, 5′-Monophosphate Levels afterin VitroRelaxin Incubation*