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. Intracranial injections of the individual components of the renin-angiotensin system caused drinking in water-replete dogs. 2. Angiotensin II was the most reliable, potent and rapidly acting intracranial dipsogen and elicited drinking in the absence of peripheral circulatory changes. After the highest dose of angiotensin II (10(-9) mole) five dogs drank a mean amount of 380.0 +/- 88.6 ml. For the other components, the order of dipsogenic effectiveness was angiotensin I, synthetic renin substrate, and angiotensin III. 3. Isotonic saline, bradykinin (10(-10) mole), eledosin-hexapeptide (10(-10) mole), oxytocin (10(-10) mole) and prostaglandin F2alpha (1-200 X 10(-12) mole) were ineffective. 4. Intracranial renin (10 m-u.) produced a mean intake of 445 +/- 152 ml. of water in eight dogs. 5. Dog renin substrate and synthetic renin substrate, injected intracranially in a dose of 10(-10) mole, produced similar intakes of water but these amounts were very much less than the volume drunk in response to the same dose of angiotensin II. 6. None of the components injected into dipsogenically responsive sites in the brain caused changes in blood pressure, although the act of drinking itself produced a small rise. 7. Angiotensin II at the highest dose produced drinking when injected into the subfornical organ, preoptic region, anterior hypothalamus, lateral ventricle, third ventricle, ventral hippocampus and mid-line thalamus. Negative sites were found in the caudate nucleus, fourth ventricle, mid-brain, posterior thalamus, dorsal hippocampus, lateral hypothalamus and posterior hypothalamus. 8. After the lowest dose of intracranial angiotensin II (10(-12) mole) only the preoptic region and subfornical orgal were responsive. These two sites were equally sensitive in terms of latency and amounts drunk at all doses injected. 9. Angiotensin did not necessarily have to reach a cerebral ventricle in order to cause drinking. 10. The dog resembles the rat in its responsiveness to the dipsogenic action of intracranial angiotensin II. The regions of the brain from which drinking can be elicited are more widespread than has been claimed by some in the rat.
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PMID:Drinking and haemodynamic changes induced in the dog by intracranial injection of components of the renin-angiotensin system. 65 Apr 66

Angiotensin II (ANG II) acts peripherally as a hormone, with actions on the vasculature, adrenals, and kidney. In addition, certain actions of ANG II in the central nervous system are directed toward cardiovascular control and fluid volume homeostasis. Dense binding sites for ANG II are found at circumventricular organs, which apparently have the ability to relay information to cardiovascular centers via neural circuitry. Microinjection of ANG II into the subfornical organ (SFO) or area postrema (AP) produces site-specific increases in blood pressure. In addition, electrophysiological studies demonstrate profound effects of ANG II, acting at the SFO, on activity of neurohypophysial neurons and release of oxytocin and vasopressin, which can be antagonized by ANG II blockers or attenuated by SFO lesions. Evidence from microinjection, electrophysiological, and lesion studies indicate a complex interaction between central sites involved in mechanisms of cardiovascular control: the SFO, AP, organum vasculosum of the lamina terminalis, and paraventricular and supraoptic nuclei of the hypothalamus. Not only is ANG II a humoral messenger in this central scenario, but evidence suggests it acts as a neurotransmitter or neuroendocrine substance within specific CNS pathways, suggesting multiple roles for this peptide in central cardiovascular control.
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PMID:Central actions of angiotensin in cardiovascular control: multiple roles for a single peptide. 142 21

Specimens of the human uterine artery and its branches were taken at hysterectomy. By microscopical dissection, three groups of arteries were obtained with respect to size-main stem, medium and small branches (inner diameters of greater than 1, 0.6-0.8 and less than 0.4 mm, respectively). The contractile effects of different vasoactive substances were studied and the responses expressed as percentages of that of K(+)-depolarization calculated. The most potent vasoconstrictor (the lowest EC50 concentration) was arginine vasopressin (AVP) followed in order by endothelin, oxytocin, prostaglandin (PG)F2 alpha, noradrenalin and dopamine. Angiotensin had inconsistent effects. Atrial natriuretic peptide (ANP) counteracted the contractile effects of endothelin. AVP, endothelin, oxytocin and noradrenalin were significantly more potent on the smallest branches than on the main stem of the artery. Since the former type of vessel represents resistance arteries, the present results suggest that AVP, endothelin, oxytocin and noradrenalin could be of specific importance in the regulation of uterine blood flow. PGF2 alpha, dopamine and angiotensin appear to be of minor importance from this aspect but ANP could play a role by regulating the effects of endothelin.
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PMID:Differences in vasomotor responses between main stem and smaller branches of the human uterine artery. 176 5

The synthesis and release of PRL are regulated by a variety of factors that originate in the hypothalamus, peripheral tissues, or posterior pituitary (PP). We recently reported that coculture of anterior pituitary (AP) and PP cells induced an increase in both PRL cell content and the responsiveness of lactotrophs to TRH. The aim of the present study was to determine whether the augmented response to TRH is due to increased lactotroph sensitivity to this particular secretagogue or to enhancement of the releasable pool of PRL. Cells obtained from anterior pituitaries of adult male rats were plated either alone or together with PP cells at the same total density. Cells cultures were maintained in serum-free medium for 4 days and then incubated for 20 min with the designated substances. Angiotensin-II and TRH evoked a significantly larger release of PRL in AP + PP cocultures than in AP cells cultured alone; the greatest difference between the culture types was observed at the highest concentrations of both secretagogues. The stimulation of PRL release by KCl, the calcium ionophore A23187, and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate was higher in the presence of PP cells than in cultures of AP cells alone, although the magnitude of this effect was lower than that seen with PRL secretagogues. The concomitant application of A23187 and 12-O-tetradecanoylphorbol-13-acetate resulted in an increased response in both types of culture and a greater relative effect of PP cells on the evoked PRL release. In contrast to other secretagogues, oxytocin (OT) elicited a smaller response in AP + PP cocultures than in AP cultures. OT was present in significant amounts in medium from cocultures, apparently after being released from the severed neuronal terminals. When AP cultures were pretreated for 4 days with comparable concentrations of OT, the acute OT-evoked PRL release was greatly diminished. These findings suggest that coculture with PP cells increases the releasable pool of PRL in lactotrophs. The stored PRL is accessible for release by secretagogues known to act via the Ca2+ second messenger system, involving both Ca2+/calmodulin and protein kinase-C pathways. The diminished response of cocultures to OT is probably due to desensitization of lactotrophs by the residual amounts of this peptide present in the disrupted nerve endings.
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PMID:Effects of coculture of anterior and posterior pituitary cells on the responsiveness of lactotrophs to different secretagogues. 193 84

We studied trophic effects of angiotensin II, vasopressin and oxytocin on explanted ventral spinal cord cultures derived from 13 to 14-old day rat embryos. There was a significant neurite promoting effect in angiotensin II and vasopressin-treated cultures. Angiotensin II had the most potent effect at any concentrations. It became clear that minimum effective concentration was 10(-8)M in both angiotensin II and vasopressin. However, oxytocin had no neurotrophic effect at any concentrations. Our results demonstrated that angiotensin II and vasopressin have a neurotrophic effect on ventral spinal cord in cultures, and may contribute to therapeutic strategy of amyotrophic lateral sclerosis.
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PMID:[Trophic effect of angiotensin II, vasopressin and oxytocin on the ventral spinal cord of rat embryo]. 227 65

The substances stimulating the release of immunoreactive corticotropin-releasing factor from cultured human placental cells were investigated. Monolayer primary cultures of trophoblast cells from pregnant women at term were used. The immunoreactive corticotropin-releasing factor released in the culture medium eluted from high-performance liquid chromatography with the same retention time as human corticotropin-releasing factor. Norepinephrine and acetylcholine increased immunoreactive corticotropin-releasing factor release into the culture medium in a dose-related manner. Epinephrine was partially active, whereas dopamine and serotonin did not induce significant changes of immunoreactive corticotropin-releasing factor release from placental cultures. Angiotensin II, interleukin-1, oxytocin, and arginine-vasopressin also increased placental immunoreactive corticotropin-releasing factor release in a dose-related manner, whereas other peptides (vasoactive intestinal peptide, substance P, somatostatin, atrial natriuretic factor, interleukin-2) were ineffective. These results showed that several neurotransmitters and peptides stimulate the release of immunoreactive corticotropin-releasing factor from placental cells, suggesting their possible involvement in the physiologic regulation of placental immunoreactive corticotropin-releasing factor release during pregnancy and parturition.
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PMID:Neurotransmitters and peptides modulate the release of immunoreactive corticotropin-releasing factor from cultured human placental cells. 256 97

We studied trophic effects of angiotensin II, vasopressin and oxytocin on explanted ventral spinal cord cultures from 13-14-old day rat embryos. There was a significant neurite promoting effect in angiotensin II and vasopressin-treated cultures. Angiotensin II had the most potent effect at any concentrations. It became clear that minimum effective concentration was 10(-8) M in angiotensin II and vasopressin respectively. Effect of these two neuropeptides was concentration-dependent. However, oxytocin had no neurotrophic effect at any concentrations. Our results demonstrated that angiotensin II and vasopressin have a neurotrophic effect on ventral spinal cord in cultures, and may contribute to therapeutic strategy of amyotrophic lateral sclerosis.
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PMID:Neurotrophic effect of angiotensin II, vasopressin and oxytocin on the ventral spinal cord of rat embryo. 258 29

1. Pressure changes in the submaxillary and parotid ducts of dogs, induced by nerve stimulation or intravenous injection of drugs, were studied.2. Pressure rises could be elicited by parasympathetic stimulation and by acetylcholine and methacholine, even when no secretion was evoked. These effects were abolished by atropine.3. Similarly, sympathetic stimulation, adrenaline, noradrenaline and phenylephrine raised the pressure in both glands, also in the absence of secretion. Dihydroergotamine abolished these effects. Isoprenaline increased the pressure in the submaxillary duct, but only when it caused secretion. This effect was abolished by propranolol. In the parotid gland isoprenaline caused neither secretion nor pressure rise. It is concluded that the myoepithelial cells of the two glands are supplied with alpha-adrenoceptors.4. Doses of histamine, bradykinin, kallidin and physalaemin which caused no salivary secretion raised the duct pressure even when dihydroergotamine, propranolol and atropine had been given.5. Angiotensin and 5-hydroxytryptamine increased the pressure only in some experiments. Oxytocin caused very little or no pressure rise. Vasopressin had no effect of its own but reduced the pressure raising effects of nerve stimulation or drugs.
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PMID:The pharmacology of salivary myoepithelial cells in dogs. 534 69

The present study investigated whether specific [3H]oxytocin binding sites previously demonstrated in estrogen-dominated rabbit uterus have properties expected of physiologic receptors coupled to uterine contraction. Microsomal membranes from estrogen-dominated rabbit uterus were found to contain high-affinity specific oxytocin binding sites with Kd = 2-3 nM. These sites were predominantly myometrial in locus. Specific oxytocin binding exhibited a pH optimum between 7.5 and 8.0. Mg2+ or Mn2+ was necessary for maximal specific [3H]oxytocin binding; in contrast, Ca2+ at submillimolar concentrations inhibited specific binding. Oxytocin binding sites were not detectable in microsomal membranes isolated from progesterone-dominated rabbit uterus. Relative binding and uterotonic activities of 10 synthetic neurohypophyseal hormone analogues were determined in estrogen-dominated rabbit uterus. A qualitative correlation was observed between binding and uterotonic responses. Angiotensin II and insulin did not compete with [3H]oxytocin for uterine binding sites. It is concluded that the specific high affinity [3H]oxytocin binding sites demonstrated in estrogen-dominated rabbit uterus have the selectivity for neurohypophyseal hormone analogues expected for physiologic receptors coupled to uterine contraction.
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PMID:Oxytocin receptors coupled to uterine contraction in estrogen-dominated rabbits. 624 2

The effect of leucine5 -enkephalin on angiotensin II (AII)-stimulated release of oxytocin and vasopressin (VP) was investigated in the conscious male rat. Changes in the plasma concentration ([]) of both oxytocin and VP were measured in animals: (1) 60 s after intracerebroventricular (i.v.t.) administration of either artificial cerebrospinal fluid (CSF) or CSF with AII (10, 50, 100 ng/5 microliter); (2) 30, 60, 90 and 300 s after single injection of AII (50 ng/5 microliter; i.v.t.) or CSF and (3) 60 s after AII (50 ng/5 microliter) or CSF in animals pretreated with leucine5 -enkephalin (100 ng/5 microliter; i.v.t.) or CSF (5 microliter). Oxytocin and VP were quantified by radioimmunoassay and values corrected for 100% recovery. The development of a sensitive radioimmunoassay for oxytocin is described. The antiserum for oxytocin enabled detection of greater than or equal to 0.8 pg/ml oxytocin with cross-reactivity of 0.01% with arginine vasopressin and 0.10% with arginine vasotocin. The inter- and intra-assay coefficients of variation were 3-9% and 3.2%, respectively. The hypotheses being tested were that i.v.t. injection of AII stimulates release of both neurohypophysial hormones non-selectively and that leucine5 -enkephalin inhibits both AII-stimulated oxytocin and VP release. Angiotensin II at doses ranging from 10 to 100 ng/5 microliter, i.v.t. increased the plasma concentration of both oxytocin and VP. Plasma levels of both neurohypophysial hormones were elevated 30 s after AII administration i.v.t. and remained elevated 300 sec later.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enkephalin inhibition of angiotensin-stimulated release of oxytocin and vasopressin. 672 45


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