Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasoactive intestinal polypeptide (VIP)ergic nerves innervate both the neurohypophysis and the hypothalamus. To test the hypothesis that VIP is a releasing factor for neurohypophyseal hormones, rats were given intracerebroventricular (icv) infusions of VIP in doses varying from 0.3 pmol/kg.min to 3 nmol/kg.min for 5 min (0.001-10 micrograms/rat). Serial blood samples were drawn from the vena cava for measurement of oxytocin (OT), vasopressin (AVP), and VIP by RIA. After the VIP infusions mean plasma OT and AVP levels rose in a dose-dependent manner; the rise was significant for both hormones at the dose of 300 pmol/kg.min. Peak levels after infusion of 3 nmol/kg.min were greater for OT than AVP [96.1 +/- 14.7 vs. 33.9 +/- 9 microU/ml (mean +/- SE); n = 6]. In addition, the concentration of plasma OT increased more promptly than that of AVP. Plasma OT was significantly raised over control values at 5 min, whereas plasma AVP was not increased until 15 min after the VIP infusion began. The concentration of VIP in peripheral plasma rose somewhat after icv infusions (maximum, 300 pmol/liter 30 min after 10 micrograms/rat), but the rise was only 5% of that observed after systemic infusions of equimolar doses of VIP (maximum, 6000 pmol/liter 5 min after 10 micrograms/rat). Peak plasma OT levels after administration of 3 nmol/kg.min VIP were significantly higher after icv than after systemic infusion of the same dose of VIP reported previously. Intravenous injection of 0.5 ml VIP antiserum with a binding capacity of VIP of 2.3 micrograms/ml before the icv administration of VIP (1 microgram/rat) did not prevent the VIP-induced rise in plasma OT and AVP. These observations suggest a central site of action for VIP in OT and AVP release, probably in the hypothalamus. The results are in harmony with the hypothesis that endogenous VIP is a physiological regulator of OT and AVP release in rats.
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PMID:Release of oxytocin and vasopressin by intracerebroventricular vasoactive intestinal polypeptide. 316 20

Vasopressin (VP) is synthesized as propressophysin, containing also neurophysin (NP) and C-terminal glycopeptide (CPP), within the hypothalamo-neurohypophyseal system (HNS). Recently, VP and NP-immunoreactive cells were demonstrated in other rat brain nuclei. Here we report CPP immunoreactivity in perikarya in these nuclei. Within the homozygous Brattleboro rat, known to be deficient in neuronal VP production, no CPP immunoreactivity was seen in these nuclei. However, intense VP and CPP immunoreactivity was present in solitary cells (52.2 +/- 3.3 per rat) and fibres within the HNS.
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PMID:Propressophysin is present in neurones at multiple sites in Wistar and homozygous Brattleboro rat brain. 374 11

The effect of relaxin on electrically evoked release of oxytocin from the posterior pituitary was examined by monitoring changes in intramammary pressure in the anaesthetized lactating rat. The amount of oxytocin released by electrical stimulation of the neurohypophysis in vivo was dramatically reduced following i.v. injection of highly purified porcine relaxin (2.5-10 micrograms/rat). Relaxin inhibited oxytocin release in a dose-dependent manner and the onset of inhibition occurred within 6-10 min and lasted for 10-60 min. No effect on the sensitivity of the mammary gland to exogenous oxytocin was observed after relaxin treatment. During the period of inhibition, i.v. injection of the opioid antagonist naloxone chloride (1 mg/kg) completely and immediately restored electrically evoked oxytocin release. The neurohypophysis is known to contain endogenous opioid peptides, therefore the effect of relaxin on electrically stimulated release of oxytocin from the rat isolated neural lobe in vitro was examined. Relaxin (500-2000 ng/ml) failed to inhibit oxytocin release in vitro. The results suggest that relaxin can inhibit the release of oxytocin from terminals in the neurohypophysis, but by an indirect mechanism. This action appears to be mediated through endogenous opioid peptides whose source is not clear. They are unlikely to be of neurohypophysial origin and may probably come from the adrenal medulla, since acute adrenalectomy negated the inhibitory effect of relaxin on oxytocin release.
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PMID:Effects of porcine relaxin on oxytocin release from the neurohypophysis in the anaesthetized lactating rat. 375 59

Oxytocin, either intraperitoneally injected (200 ng/rat) or intracerebroventricularly infused (1 ng/rat in 4 microliters saline) 60 and 15 min respectively before testing, significantly increased the lordosis response to the mounting male of ovariectomized, estrogen/progesterone treated rats. The intracerebroventricular infusion of oxytocin 0.1 ng/rat had no effect; nor did saline. These results indicate that oxytocin increases female receptivity, the site of action probably being in the central nervous system.
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PMID:Oxytocin stimulates lordosis behavior in female rats. 402 80

1. The exteroceptive stimulus emanating from a lactating rat and the litter while suckling was used to induce milk ejection in another lactating mother 15 min before the replacement of her own litter. The effect of the external stimulus on milk ejection during one 30 min period and four 15 min periods of nursing was studied.2. After being isolated for 9 hr the litter from the mother subjected to the exteroceptive nursing stimulus (induced rat) obtained a significantly greater amount of milk during 30 min of nursing than that obtained by the litter from the control mother.3. When deaf mother rats were used the gain of milk by the litter showed no difference between the control and the induced mother. This result indicated that the effective external stimulus is an auditory one and is probably produced by the mother rat and the young while suckling.4. The administration of oxytocin (Syntocinon, Sandoz) 20 m-u./100 g body wt., 15 min before the replacement of the litter produced a milk ejection similar to that obtained under the influence of the auditory stimulus. This would indicate that the exteroceptive stimulus probably evokes the release of oxytocin from the neurohypophysis.5. When nursing was performed in four periods of 15 min each the litter of the control mother obtained milk only in the second period of nursing while the litter of the induced mother obtained milk in all four periods of nursing and the amount of milk obtained in the whole hour was greater than that from the control rat.6. The administration of oxytocin just before the replacement of the litter every 15 min produced milk ejection only in the first two periods of suckling in the control rats but the induced rats were capable of ejecting milk during all four periods.7. The most satisfactory conclusion for the results obtained is that the C.N.S. regulates both the release of oxytocin in response to suckling and the response of the mammary gland to oxytocin, in the lactating rat.
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PMID:The effect of an exteroceptive stimulus on milk ejection in lactating rats. 569 44

Specific SRIF(1-14) fragments were synthetized on resin using conventional procedures. Rabbits received subcutaneously peptidyl resins in complete Freund adjuvant emulsion. The presence of antibodies was assessed by immunocytochemical and radioimmunological assays. 1. Peptidyl resins lead to antibodies production; their specificity depends on sequence and molecular configuration of the peptide on the resin. Anti-resin antibodies were not detected. 2. In the brain, SRIF(1-4) (in rat) and SRIF(10-13) (in garden-dormouse) can be demonstrated in neurophysins--positive cells of both paraventricular and supraoptic nucleus, but never in hypothalamic or extrahypothalamic SRIF(1-14)--positive neurophysin negative cells. 3. Endocrine cells of pancreatic islets contain SRIF(6-9) (in man) or SRIF(10-13) (in rat, mouse, garden-dormouse); generally, these cells are not detected by SRIF(1-14) anti-serum. Moreover, SRIF(10-13) positive cells are also detected by specific glucagon antibodies. However, it cannot be concluded that SRIF(10-13) antibodies reveal the common Thr-Phe-Thr-Ser fragment in the entire glucagon molecule. It is postulated that antibodies to several SRIF tetrapeptides reveal molecular fragments provided by the functional cleavage of an hypothetical prohormone or by the inactivation of SRIF(1-14) molecule in target cells.
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PMID:[Preparation of antisera against some sequences of somatostatin synthetized on resin. Application to the immunological detection of somatostatin systems: preliminary results (author's transl)]. 612 35

Adult male rats were implanted with transcutaneous ECG electrodes and habituated to a dark chamber with elevated background noise levels. ECG was recorded prior to, immediately after, and 3 min after sudden elimination of background noise. The orienting response to the stimulus offset was accompanied by transient bradycardia. Neither AVP (1 microgram/rat) nor oxytocin (1 microgram/rat) injected subcutaneously 1 hr prior to testing altered baseline heart rate or the immediate bradycardiac response to stimulus offset. However, AVP, and to a lesser extent oxytocin, prolonged the bradycardia induced by stimulus offset. The results show that neurohypophyseal peptide hormones enhance the cardiovascular component of orienting to stimulus change.
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PMID:Vasopressin prolongs bradycardiac response during orientation. 646 69

In several species the myometrium is quiescent shortly before parturition. At this time high titres of relaxin are present in the plasma and there is evidence that the hormone has a direct inhibitory action on the uterine muscle. Relaxin could also contribute to uterine quiescence by inhibiting oxytocin release. To determine whether relaxin has a central action on the release of oxytocin, we have studied the effect of intravenous injections of porcine relaxin on milk ejection in the anaesthetized lactating rat. We report that reflex milk ejection was suppressed by relaxin in a dose-dependent manner, the onset of inhibition being rapid and lasting from 10 to 60 min. After the period of inhibition the normal temporal pattern of reflex milk ejection was resumed. Mammary sensitivity to exogenous or endogenous oxytocin was reduced by relaxin but not sufficiently to explain the effects observed. Furthermore, relaxin (1 microgram per rat) injected into the cerebral ventricles profoundly disturbed the pattern of reflex milk ejection without affecting the response of the mammary gland to oxytocin. These results suggest a novel role for relaxin within the central nervous system. The site in the brain at which the effects of relaxin are exerted remains unknown.
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PMID:Relaxin affects the central control of oxytocin release. 672 91

RIAs have been developed for the nonapeptide hormones arginine vasotocin (AVT), arginine vasopressin (AVP), and oxytocin (OT). The AVP RIA can detect as little as 2 pg hormone and shows essentially no cross-reactivity with AVT or OT. The OT RIA is sensitive to 7 pg and shows no significant cross-reactivity with AVP or AVT. The AVT RIA is sensitive to about 5 pg; some cross-reactivity occurs with OT and AVP, but the RIA is suitable for assaying AVT levels in biological samples containing OT and/or AVP in concentrations up to 5 times greater than that of AVT. Using these RIAs, we found large amounts of AVT (up to 1.48 microgram/gland) in the chicken pituitary but no AVP or OT. The chicken pineal also contained AVT (about 300 pg/gland) and lacked AVP and OT. Bovine pineal glands appeared to contain all three peptides in roughly similar amounts (200-400 pg/gland). Pineal glands from a variety of rodents (including the rat) contained only very small amounts of AVT-like immunoreactivity (about 10 pg/gland) and no AVP or OT. Because AVT immunoreactivity appears in the pineals of several species, the peptide may subserve some physiological function of this organ. The functional roles, if any, of AVP and OT in the bovine pineal are unknown.
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PMID:Radioimmunologic detection and measurement of nonapeptides in the pineal gland. 734 56

The general pharmacological study of iodixanol, a non-ionic isotonic contrast medium, was conducted. 1) Iodixanol administered intravenously over a dose range of 320 to 3,200 mgI/kg had little or no effect on the general behavior, spontaneous locomotor activity, hexobarbital sleeping time, pain response, electroshock- or pentylenetetrazol-induced convulsion (mouse), EEG or body temperature (rabbit), gastrointestinal propulsion (mouse) or skeletal muscle contraction (rabbit). Iodixanol had no specific interaction with acetylcholine, histamine, serotonin, nicotin, BaCl2 (ileum), methacholine (trachea), isoprenaline (atrium) or oxytocin (pregnant uterus), nor had any effect on spontaneous contractility (atrium and uterus), or transmural electrostimulation-induced contractility (vas deferens) at concentrations of < or = 3.2 x 10(-3) gI/ml in vitro. Iodixanol had no effect on the cardiovascular system of dog, except that it increased femoral blood flow and respiratory rate at doses of > or = 1,000 mgI/kg. Iodixanol at 3,200 mgI/kg i.v. reduced urine output with a decrease in Na+ and Cl- excretion, whereas at 320 mgI/kg i.v., it slightly increased urine output (rat). 2) Injections of iodixanol into the cerebroventricular (0.96, 9.6 mgI/mouse and 3.2, 32 mgI/rat), left ventricular (1,920, 6,400 mgI/dog) or coronary artery (640, 1,920 mgI/dog) had no conspicuous effect on the central nervous system or the cardiovascular system, respectively. There was no marked difference among iodixanol, iohexol and iopamidol in this respect. Vascular pain during injection into the femoral artery (300-320 mgI/guinea pig) appeared to be less intense with iodixanol, compared with the other contrast media iohexol and iopamidol. These results suggest that intravenous injection of iodixanol is relatively free from pharmacological activity, and effects of iodixanol on the central nervous system (intracerebroventricular injection) and cardiovascular system (intra-left ventricular and -coronary injections) are comparable to those of iohexol and iopamidol. Furthermore, intra-femoral injection of iodixanol has less of a tendency to produce vascular pain than those of iohexol and iopamidol.
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PMID:[General pharmacological study of iodixanol, a new non-ionic isotonic contrast medium]. 749 Jul 85


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