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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The current study tested the hypothesis that centrally administered relaxin elevates arterial pressure in conscious rats and that this hypertensive effect is mediated, at least in part, by central or peripheral vasopressin. Injection of human relaxin (0.068 or 0.34 microgram in 200 nL artificial cerebrospinal fluid) into the right lateral ventricle of conscious, unrestrained Sprague-Dawley rats caused significant dose-related increases in arterial pressure and decreases in heart rat. The pressor and bradycardic responses to intracerebroventricular injections of relaxin were significantly blunted by pretreatment with either intracerebroventricular or intravenous injection of a vasopressin receptor (V1) antagonist, suggesting that the cardiovascular effects of central relaxin are mediated, at least in part, by V1 receptors in the brain and perhaps also by vasopressin released into the peripheral circulation. Neither intracerebroventricular injection of the vehicle alone nor intravenous injection of relaxin (0.34 microgram) altered arterial pressure or heart rate. In contrast to the above, intravenous injections of relaxin (40 micrograms/kg) elicited pressor and tachycardic responses that were not blunted by pretreatment with either intracerebroventricular or intravenous injection of the V1 receptor antagonist. Together, these data suggest that in the central nervous system relaxin contributes to the regulation of cardiovascular function and that the mechanisms for the cardiovascular effects of central and peripheral relaxin are distinct.
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PMID:Pressor and bradycardic effects of centrally administered relaxin in conscious rats. 761 50

Relaxin is known for its function in parturition and has been suggested to participate in the regulation of blood pressure, heart rate, and the release of neuropeptides such as oxytocin and vasopressin. Consistent with the physiological roles of relaxin, high affinity relaxin receptors have been demonstrated in the rat uterus, brain, and cardiac atrium. Here we report the binding and cross-linking of a biologically active, 32P-labeled human relaxin to a human uterine cell line and primary rat atrial cardiomyocytes. Relaxin binding to the human uterine cells consisted of a single class of high affinity sites (Kd = approximately 0.44 nM) with approximately 1082 +/- 62 binding sites/cell. Binding and cross-linking of relaxin to the human uterine cells and rat atrial cardiomyocytes followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis revealed that the putative relaxin receptor showed a major component with an apparent M(r) greater than 220 kilodaltons and a minor component of approximately 36 kilodaltons, and was not disulfide linked. The binding and cross-linking of [32P]relaxin could be displaced by unlabeled relaxin in a concentration-dependent manner, but not by a 1000-fold molar excess of insulin, insulin-like growth factor I (IGF-I), or IGF-II. These data suggested that the relaxin receptor was similar in size but distinct from the insulin, IGF-I, and IGF-II receptors.
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PMID:Binding and cross-linking of 32P-labeled human relaxin to human uterine cells and primary rat atrial cardiomyocytes. 766 57

This review stresses changes in osmoregulation as well as the secretion and metabolism of arginine vasopressin during pregnancy, focusing on human gestation. Pregnant women experience a decrease in body tonicity, plasma osmolality decreasing immediately after conception to a nadir approximately 10 mosmol/kg below non-pregnant levels early in pregnancy, after which a new steady state is maintained until term. Data from both human and rodent gestation have led to a formation of how these changes occur. The osmotic thresholds for thirst and antidiuretic hormone release decrease in parallel. Lowering the threshold to drink stimulates increased water intake and dilution of body fluids. Because arginine vasopressin (AVP) release is not suppressed at the usual level of body tonicity, the hormone continues to circulate and the ingested water is retained. Plasma osmolality declines until it is below the osmotic thirst threshold, and a new steady state with little change in water turnover is established. Pregnancy is characterized by increments in intravascular volume, but volume-sensing AVP release mechanisms appear to adjust as gestation progresses so that each new volume status is "sensed" as normal. The metabolic clearance of AVP increases fourfold, the rise paralleling that of circulating cystine aminopeptidase (vasopressinase), and enzyme produced by the placenta. Furthermore, the disposal rate of 1-deamino-8-D-AVP, and AVP analogue resistant to inactivation by vasopressinase, is unaltered in pregnancy. Thus, the increase in AVP's metabolism and the high circulating aminopeptidase levels have been implicated in certain forms of transient diabetes insipidus that occur in late pregnancy. Finally, mechanisms responsible for the altered osmoregulation in pregnancy are obscure, but chorionic gonadotropin and relaxin may be implicated in the changes.
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PMID:Osmoregulation, the secretion of arginine vasopressin and its metabolism during pregnancy. 785 29

Experiments were done to study the effects of porcine relaxin on osmotically evoked changes in intramammary pressure and the release of oxytocin and vasopressin in anaesthetized rats. Injections (1 microliter) of hypertonic (0.75 M) NaCl into the left lateral cerebral ventricle were used to induce consistent rises in intramammary pressure and the release of oxytocin and vasopressin. Plasma hormone concentration was determined by radioimmunoassay. Relaxin (5 micrograms i.v.) significantly (P < 0.05) suppressed the intramammary pressure response to osmotic challenge 5 and 10 min after treatment. However, pretreatment with a specific vasopressin V1 receptor antagonist completely negated the effect of relaxin on intramammary pressure. Baseline levels of oxytocin and vasopressin in unstimulated rats were 41 +/- 1.6 and 36 +/- 1.1 pmol/l respectively. Osmotic challenge induced significant (P < 0.05) rises in plasma levels of both hormones (62.8 +/- 1.1 and 67.9 +/- 1.2 pmol/l respectively) which were further augmented by relaxin (81.3 +/- 1.8 and 117.1 +/- 2.4 pmol/l respectively; P < 0.05). The data confirm that central osmotic challenge provokes the release of oxytocin and vasopressin but the effects of oxytocin at the level of the mammary gland may be obscured by the action of vasopressin affecting blood flow to the gland.
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PMID:Effects of exogenous relaxin on oxytocin and vasopressin release and the intramammary pressure response to central hyperosmotic challenge. 801 6

Experiments were conducted in anesthetized rats to assess the contribution of the brain angiotensin-II system in the relaxin-induced secretion of vasopressin and oxytocin. Intravenous injection of porcine relaxin (5 micrograms) caused a significant (P < 0.05, by analysis of variance) increase in plasma concentrations of both hormones. Peak concentrations of both vasopressin (75.2 +/- 2.9 pmol/liter) and oxytocin (38.4 +/- 1.2 pmol/liter) were observed 1-2.5 min after relaxin injection. Thereafter, concentrations fell significantly (P < 0.05) but remained elevated for a further 25 minutes. Continuous infusion of a specific angiotensin-II receptor antagonist into the lateral cerebral ventricle did not affect baseline levels of either vasopressin or oxytocin, but did significantly reduce (P < 0.05) the relaxin-induced release of both peptides. A significant (P < 0.05) short term increase in both plasma vasopressin and oxytocin occurred 1 min after injection of 5 micrograms relaxin, iv, in angiotensin-II-antagonized rats, but the concentrations of both neuropeptides were significantly (P < 0.05) lower than those observed in the angiotensin-intact relaxin-treated controls. These data suggest that relaxin may act through the central angiotensin-II system to induce the release of vasopressin and oxytocin.
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PMID:Brain angiotensin-II partially mediates the effects of relaxin on vasopressin and oxytocin release in anesthetized rats. 811 58

The effects of porcine relaxin (pRXN) on arterial blood pressure and on the release of vasopressin (VP) and oxytocin (OT) were investigated in urethane-anesthetized rats at different stages of pregnancy and lactation. Acute i.v. pRXN (5 micrograms) caused a significant increase in systolic and diastolic blood pressure in pregnant and lactating rats. However, the pressor response was attenuated from Day 14 of pregnancy to Day 1 of lactation. The hormone had no effect on blood pressure in Day 16, Day 19, or Day 21 pregnant rats. At all stages of pregnancy and lactation, i.v. pRXN caused a significant increase in plasma VP concentrations. This response was attenuated in Day 19 and Day 21 pregnant and in Day 1 lactating rats. Intravenous pRXN also caused a significant, short-term increase in plasma OT in pregnant and lactating rats. The OT response to pRXN was attenuated on Day 16 of pregnancy, and pRXN had no effect on plasma OT in late-pregnant rats. The data in this study demonstrate that pRXN causes an increase in both arterial blood pressure and VP and OT release in anesthetized pregnant and lactating rats. However, these effects are either reduced or not observed in late-pregnant and early-lactating rats.
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PMID:Effects of relaxin on blood pressure and the release of vasopressin and oxytocin in anesthetized rats during pregnancy and lactation. 816 34

Relaxin is a polypeptide hormone best known for its role in parturition. However, high affinity relaxin receptors have been localized in the rat brain and heart in addition to the uterus. Several lines of evidence also suggest that relaxin may be involved in the regulation of blood pressure, heart rate, and the release of oxytocin and vasopressin. We now show by Northern analysis that a 1-kilobase relaxin transcript is detected in the rat brain as well as the ovary of pregnant rats. Using in situ hybridization, relaxin mRNA is localized in discrete regions of the male and female brains, including the anterior olfactory nucleus, tenia tecta, pyriform cortex, neocortex, and hippocampus. Developmental studies show that relaxin mRNA is present in the 1-day postnatal brain, while relaxin receptors are not detectable until 7 days after birth. The relaxin receptor binding affinity was similar in the developing brains, but there was a steady increase in relaxin binding sites during postnatal days 7 to 29, suggesting that relaxin may play a role in brain maturation. While relaxin mRNA is not detected in the heart, high levels of relaxin receptors are detected in the cardiac atrium as early as 1 day after birth. These atrial receptors remained at similar levels throughout postnatal development, suggesting an important role for relaxin in cardiovascular function.
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PMID:Expression of relaxin mRNA and relaxin receptors in postnatal and adult rat brains and hearts. Localization and developmental patterns. 839 68

1. The subfornical organ, median preoptic nucleus and the organum vasculosum of the lamina terminalis (OVLT) are a series of structures situated in the anterior wall of the third ventricle and form the lamina terminalis. The OVLT and ventral part of the median preoptic nucleus are part of a region known as the anteroventral third ventricle region. 2. Data from many laboratories, using techniques ranging from lesions, electrophysiology, neuropharmacology, Fos expression, immunohistochemistry and receptor localization, indicate that the tissue in the lamina terminalis plays a major role in many aspects of body fluid and electrolyte balance. 3. The subfornical organ and OVLT lack the blood-brain barrier and detect alterations in plasma tonicity and the concentrations of circulating hormones such as angiotensin II and possibly atrial natriuretic peptide and relaxin. 4. This information is then integrated within the lamina terminalis (probably in the median preoptic nucleus) with neural signals from other brain regions. The neural output from the lamina terminalis is distributed to a number of effector sites including the paraventricular (both parvo- and magno-cellular parts) and supraoptic nuclei and influences vasopressin secretion, water drinking, salt intake, renin secretion, renal sodium excretion and cardiovascular regulation.
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PMID:Anteroventral wall of the third ventricle and dorsal lamina terminalis: headquarters for control of body fluid homeostasis? 871 61

Relaxin is a 6-kDa peptide of the insulin family that is present at increased levels in the circulation during pregnancy. Its functions at that time are thought to include maintenance of myometrial quiescence, regulation of plasma volume, and release of neuropeptides, such as oxytocin and vasopressin. The protein also promotes connective tissue remodeling, which allows cervical ripening and separation of the pelvic symphysis in various mammalian species. In this report, we provide evidence for a novel target of relaxin, the human monocytic cell line, THP-1. Relaxin bound with high affinity (Kd = 102 pM) to a specific receptor on THP-1 cells. Receptor density was low ( approximately 275 receptors/cell), but binding of relaxin triggered intracellular signaling events. Receptor density was not modulated by pretreatment with estrogen, progesterone, or a number of other agents known to induce differentiation of THP-1 cells. Cross-linking studies showed radiolabeled relaxin bound primarily to cell surface proteins with an apparent molecular mass of >200 kDa. Other members of the insulin-like family of proteins (insulin, insulin-like growth factors I and II, and relaxin-like factor) were unable to displace the binding of relaxin to THP-1 cells, suggesting that a distinct receptor for relaxin exists on this monocyte/macrophage cell line.
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PMID:Relaxin binds to and elicits a response from cells of the human monocytic cell line, THP-1. 891 Mar 95

The effect of intracerebroventricular (ICV) injections of synthetic human or rat relaxin (25 or 250 ng) on the distribution of Fos detected immunohistochemically in the rat forebrain was investigated. Following ICV relaxin, many Fos-positive neurons were observed in the periphery of the subfornical organ, dorsal part of the organum vasculosum of the lamina terminalis, throughout the median preoptic nucleus, supraoptic nucleus and hypothalamic paraventricular nucleus. Such effects did not occur following ICV injection of artificial cerebrospinal fluid or the separated A and B chains of relaxin, nor following the intravenous injection of 250 ng of relaxin. Both vasopressin and oxytocin containing neurons identified immunohistochemically in the supraoptic and paraventricular nuclei exhibited Fos following ICV relaxin, and many neurons in the medial parvocellular part of the paraventricular nucleus contained Fos. The results indicate that centrally administered relaxin may increase neuronal activity in regions of the hypothalamus and lamina terminalis which are associated with cardiovascular and body fluid regulation and oxytocin secretion.
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PMID:Distribution of Fos immunoreactivity in the lamina terminalis and hypothalamus induced by centrally administered relaxin in conscious rats. 922 54


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