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)

1. Extracellular recordings were made from 297 spontaneously firing neurones in the dorsal motor nucleus of the vagus (DMV) in slice preparations of rat medulla oblongata. Some of the neurones recorded were identified to be vagal motoneurones by antidromic stimulation. The cells fired with a slow irregular pattern at an average rate of 1.1 +/- 0.1 spikes/s (mean +/- S.E.M.). 2. Arginine vasopressin (AVP) was applied by perfusion in 196 of the 297 cells. Most of the neurones (190/196, 97%) were excited by 10(-6) M AVP with an increase in firing rate from the basal level of 1.1 +/- 0.1 to a maximum of 2.5 +/- 0.2 spikes/s. There was a dose-dependent relation between the concentration of AVP and the increased firing rate in all DMV neurones tested (n = 38). The threshold concentration of the peptide to produce changes in firing rate was assumed to be about 10(-10) M. The remaining six neurones were not affected by application of AVP. 3. Application of oxytocin (OXT, 10(-6) M) increased the firing rate of all thirty-eight neurones tested. The effects of AVP and OXT on all neurones examined (n = 20 and 4, respectively) still persisted after blocking the synaptic transmission in a low-Ca2+ or Ca(2+)-free-high-Mg2+ solution, indicating the direct action of both AVP and OXT on the postsynaptic membranes. 4. The AVP-induced excitatory responses were completely but reversibly blocked by the V1-type receptor antagonists, [1-(beta-mercapto-beta, beta-cyclopentamethylene-propionic acid), 2-(O-methyl)tyrosine]-arginine vasopressin (d(CH2)5Tyr(Me)AVP) (n = 5) and Phaa-D-Tyr(Et)Phe-Gln-Asn-Lys-Pro-Arg-NH2 (n = 6), whereas a selective and reversible OXT receptor antagonist, desGly-NH2d(CH2)5[Tyr-(Me)2Thr4]ornithine vasotocin, which suppressed the OXT-induced excitation, did not block the responses to AVP (n = 11). 5. Application of angiotensin II (AII, 10(-6) M) to 153 neurones increased the firing rates of 60 (39%) neurones. The firing rate was increased from the basal level of 1.0 +/- 0.1 to a maximum of 1.8 +/- 0.2 spikes/s (n = 60). The effect of AII was completely abolished by an AII receptor antagonist, [Sar1,Ile8]angiotensin II (n = 6). There was a dose dependence of the excitatory response on AII concentration in all of eleven neurones tested. The threshold concentration was assumed to be about 10(-9) M. The activity of 5 (3%) of 153 neurones was decreased, and the remaining 88 (58%) neurones were not affected by AII.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of vasopressin and angiotensin II on neurones in the rat dorsal motor nucleus of the vagus, in vitro. 130 79

A microperfusion system was developed to study detailed kinetics of adrenocorticotropic hormone (ACTH) secretion by dispersed rat anterior pituitary cells responding to various ACTH secretagogues. The system approaches hydrodynamics to square-wave stimuli and enables kinetic analysis of ACTH secretion with intervals as short as 5 sec. ACTH secretion initiated within 5 sec of exposure of the cells to corticotropin-releasing factor (CRF), arginine vasopressin (AVP), oxytocin (OT) or angiotensin II (A-II) and reached a maximum within 20-40 sec. CRF induced a plateau-shaped secretion of ACTH which remained constant as long as CRF was perifused. In contrast, the ACTH secretion responding to AVP, OT and A-II rose rapidly to a peak and fell to the baseline despite continued perifusion of these agents. There were two components of ACTH secretory response to AVP and OT. AVP had synergistic effect with CRF only if it was perifused simultaneously with CRF or immediately after CRF was stopped. The ACTH secretory response to A-II was greatly diminished when cells were exposed to AVP or OT before A-II perifusion. Prior exposure to A-II had no effect on the magnitude of the ACTH secretory response to either AVP or OT. Epinephrine, nor-epinephrine, gastrin-releasing peptide, atrial natriuretic factor and cholecystokinin stimulated no significant ACTH secretion in the microperfusion system, although some of them induced ACTH secretion by same cell preparation in static culture systems.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Physiological analyses of secretory kinetics of adrenocorticotropic hormone (ACTH) from anterior pituitary cells: development and application of a microperfusion system]. 131 80

Pituitary cells, collected from five healthy dogs, were cultured and treated with various doses of ovine corticotropin-releasing hormone (CRH), arginine vasopressin (AVP), oxytocin (OT), or angiotensin II (AII) to determine which of these hypothalamic peptides affected adrenocorticotropin (ACTH) secretion. Of the 4 peptides, only CRH significantly increased ACTH secretion from cultured canine anterior pituitary cells. The lowest dose of CRH tested, 0.01 nM, significantly stimulated ACTH release. Co-addition of AVP, OT, or AII with CRH did not increase ACTH secretion beyond that caused by addition of CRH alone. Similarly, neither co-addition of AVP with OT, AVP with AII, or OT with AII significantly stimulated ACTH secretion. These results support a role for CRH in the physiologic regulation of ACTH secretion from the canine anterior pituitary, but do not support regulatory roles for AVP, OT, or AII.
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PMID:Regulation of adrenocorticotropin secretion from cultured canine anterior pituitary cells. 133 8

In several models of salt appetite in the rat, stimulated NaCl intake can be severely blunted by treatments associated with pituitary release of oxytocin (OT). Central administration of the potent dipsogen angiotensin II (ANG II) is known to elicit a limited salt appetite as well as thirst, but it has also been reported to stimulate pituitary OT secretion. These results suggest the possibility that the expression of ANG II-induced salt appetite in rats may be inhibited by a simultaneous central release of OT in response to this stimulus. To investigate this possibility, rats were given intracerebroventricular injections of OT-receptor antagonists before administration of 5 ng ANG II intracerebroventricularly in a 1-h two-bottle (water and 0.3 M NaCl) drinking test. This pretreatment resulted in a three- to fourfold potentiation of ANG II-induced saline ingestion, which was most prominent during the first 15 min of the test. OT-receptor antagonism did not, however, interfere with the dipsogenic properties of ANG II, nor did it stimulate saline ingestion alone in the absence of ANG II. Immunocytochemical studies demonstrated that central administration of ANG II at this dose caused pronounced c-fos expression in hypothalamic magnocellular OT and vasopressin neurons and also in OT neurons in parvocellular subdivisions of the paraventricular nucleus. These results therefore demonstrate that central administration of small doses of ANG II activates both magnocellular and parvocellular OT neurons in rats and indicate that some of the activated central OT pathway(s) may mediate an inhibitory effect that limits the salt ingestion induced by this treatment.
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PMID:Central oxytocin inhibition of angiotensin-induced salt appetite in rats. 133 19

Human placental aminopeptidase M and A and post-proline endopeptidase are known to act as degrading enzymes of bioactive peptides such as angiotensin II, oxytocin and endogenous opioids. We tested the effects of cortisol on the activities of human placental aminopeptidase A and M and post-proline endopeptidase using short-cultured placental tissues. From 34.5 nM to 3.45 microM of cortisol significantly increased the activities of 3 enzymes. Our present data suggest a possible important role of cortisol in the growth of human placenta via induction of placental aminopeptidases.
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PMID:Induction by cortisol of aminopeptidases production from the human placenta in tissue culture. 134 55

The brain is one of the organs where an intrinsic renin-angiotensin system (RAS) has been described. Stimulation of circumventricular or brainstem angiotensin II (Ang II) receptors engenders a distinct pattern of cardiovascular, endocrine, and behavioral responses featuring blood pressure increase, attenuation of the baroreceptor reflex, drinking, release of pituitary hormones such as vasopressin, oxytocin, and ACTH, and natriuresis. In contrast to most of the other central actions of Ang II, the natriuretic effect cannot be elicited by Ang II as a circulating hormone. Recently, we have shown that stimulation of Ang II AT-1 receptors in the circumventricular organs causes a selective release of norepinephrine (NE) in the paraventricular nucleus (PVN) and in the supraoptic nucleus (SON). As vasopressin is also released from the PVN and SON, it is possible that the Ang II-NE interaction is involved in the release of vasopressin, thereby contributing to central blood pressure regulation and volume control. Finally, a substantial body of results suggests that an overactivity of the brain renin-angiotensin system is one of the contributors to genetic hypertension. However, this idea needs further confirmation.
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PMID:Role of brain angiotensin in cardiovascular regulation. 138 68

The quantitative autoradiographic method with L-(35S)methionine was applied to investigate the effect of chronic dehydration on rates of protein synthesis in circumventricular organs (CVOs). Water deprivation for 1, 2 and 3 days causes progressive increases of protein synthesis in the subfornical organ (SFO), the area postrema, the organum vasculosum laminae terminalis and the neurohypophysis. Chronic salt ingestion with 2% NaCl in drinking water for 3 days resulted in increases of protein synthesis in the CVOs similar to those found after 3 days water deprivation, with only one exception, the SFO, in which the rise in protein synthesis was of lower amplitude after 3 days salt ingestion as compared to 3 days water deprivation. These results suggest that several circulating factors related to intracellular dehydration and the high plasma levels of the neurohormones vasopressin and oxytocin are probably important determinants of the rise of protein synthesis in circumventricular organs. Alternatively, the elevated level of blood-borne angiotensin II may well explain the higher metabolic response of the SFO following water deprivation compared to salt ingestion.
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PMID:Progressive increases of protein synthesis in the circumventricular organs during chronic dehydration in rats. 141 Apr 30

Human urine samples, purified on octadecasilyl-silica cartridges, contained immunoreactive angiotensin I, II, arginine vasopressin and oxytocin. The daily excretion of these peptides in healthy volunteers was 190.00 +/- 38.43 (n = 12), 17.48 +/- 3.09 (n = 12), 63.43 +/- 14.84 (n = 8) and 13.52 +/- 1.42 (n = 7) pmol/24 hr, respectively (mean +/- s.e.m.). Patients with a history of anaphylactoid reactions to drugs or food additives showed clinical symptoms such as urticaria, flush, nausea, dizziness and hypotension after oral provocation with cyanocobalamine, propyphenazone, acetylsalicylic acid and sodium benzoate. In five of the seven patients, angiotensin I and II were increased several fold in the urine fractions after symptoms were reported. The average increase in the urine concentration of both peptides was fourfold and 5.5-fold. In three out of five patients, the mean excretion of arginine vasopressin and oxytocin immunoreactive material was also elevated by a factor of 5.7 and 4.4, respectively. Oral provocation with a placebo failed to elicit anaphylactoid symptoms or an increase in the urine levels of angiotensin I or angiotensin II. Angiotensin I and angiotensin II-like immunoreactivity could be characterized on HPLC as Ile5-angiotensin I, Ile5-angiotensin II and angiotensin II metabolites. HPLC characterization of immunoreactive arginine vasopressin and oxytocin in two different gradient systems showed retention times different than the retention times of the corresponding synthetic standard peptides indicating that both peptides are not authentic AVP and OXT. These results suggest that angiotensin I and angiotensin II may be involved in the clinical events observed during some forms of anaphylactoid reactions.
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PMID:Urinary excretion of angiotensin I, II, arginine vasopressin and oxytocin in patients with anaphylactoid reactions. 142 42

The stimulatory effect of dopamine (DA) on the release of oxytocin (OT) in lactating rats is exerted at the D-1 DA receptor subtype. Because the neural loci mediating this effect have not been identified, the objective of the present studies was to test whether OT release in the lactating rat would be elevated after central administration of a D-1 DA receptor agonist into the third ventricle (3V) or directly into either the rostral paraventricular/anterior commissural nucleus area (PVN/ACN), the central paraventricular nucleus area, or the supraoptic nucleus (SON), all of which contain OT neurosecretory cells. Lactating rats were implanted with a stainless steel cannula directed into one of the above areas or into the arcuate-ventromedial region of the medial basal hypothalamus (MBH), or sites dorsal to the PVN/ACN or SON, which served as anatomical controls. After 6-7 days of recovery, each animal received an intra-atrial cannula for sequential blood sampling, and was used in experiments 24 h later. Animals were separated from their litters, and following a period of basal blood sampling, received central microinjections of either vehicle, the D-1 DA receptor agonist SKF-38393, or the D-2 DA receptor agonist quinpirole, and blood samples were removed periodically for 60 min. An injection of angiotensin II (Ang II, 100 ng) was made into each site as a positive control for OT release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activation of central D-1 dopamine receptors stimulates oxytocin release in the lactating rat: evidence for involvement of the hypothalamic paraventricular and supraoptic nuclei. 143 76

The firing rate and pattern of activity of neurons in the anterior commissural nucleus (ACN), which was rich in oxytocin-containing neurons, were studied electrophysiologically in hypothalamic slices. Extracellular recording showed that most ACN neurons exhibited irregular or regular continuous spontaneous unit activity. Other neurons showed short burst patterns of activity or were silent. The majority of ACN neurons were activated by bath application of angiotensin II, and a substantial number of them showed inhibitory or excitatory responses to hypertonic bathing medium. These results indicate that magnocellular neurosecretory neurons in the ACN may participate in the regulation of water balance.
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PMID:Neuronal responses of the anterior commissural nucleus to osmotic stimulation and angiotensin II in hypothalamic slices in the rat. 143 19


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