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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of vasopressin receptors of the V1 (vascular) type and of oxytocin receptors in the rat kidney was investigated using an autoradiographical approach. Rat kidney sections were incubated with tritiated vasopressin ([3H]vasopressin, 1.5 nM) or oxytocin ([3H]oxytocin, 3 nM). The ligand selectivity of the [3H]vasopressin binding sites detected was deduced from competition experiments using one selective unlabeled ligand for V2 (antidiuretic) vasopressin receptors (1-deamino-[8-D-arginine]-vasopressin, dDAVP) and one selective unlabeled ligand for V1 receptors (des-glycineamide-[1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid]-arginine vasopressin, des(Gly(NH2)9d(CH2)5-AVP). Specific and dense [3H]vasopressin labeling was observable in the medullopapillary and cortical portions of the kidney. Specific [3H]vasopressin binding in the cortex was insensitive to the V1-selective ligand, des(Gly(NH2)9d(CH2)5-AVP, but was inhibited by dDAVP. Glomerular structures identified as such by microscopical observation of the kidney sections were specifically labeled with [3H]oxytocin and [125I]-SAR1-angiotensin II but not with [3H]vasopressin. It is concluded that V1 receptors which have been evidenced on mesangial cells in culture are not expressed in a detectable quantity on mesangial cells in situ. The specific [3H]oxytocin binding to glomeruli might reflect the presence on glomerular structures of oxytocin receptors involved in the effects of the hormone on renal hemodynamics, and possibly in some of the effects ascribed to vasopressin.
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PMID:Autoradiographic localization of vasopressin and oxytocin binding sites in rat kidney. 339 84

Since neuroimmunomodulation is brought about in part, at least, by secretion of pituitary hormones involved in stress and immune responses, we review briefly the hypothalamic control of the release of ACTH, growth hormone, and prolactin. The release of ACTH is controlled particularly by corticotropin-releasing factor (CRF), but vasopressin has intrinsic releasing activity and potentiates the action of CRF at both hypothalamic and pituitary levels. Oxytocin may even potentiate the action of CRF, but has little, if any, ACTH-releasing activity by itself. In addition, epinephrine may augment responses to the CRFs. In contrast, growth hormone is under dual control by growth-hormone-releasing factor (GRF) and somatostatin, and prolactin is under multifactorial control by a series of inhibitors and stimulators. Dopamine is accepted as a physiological prolactin-inhibiting factor (PIF), but probably GABA and possibly acetylcholine as well are PIFs. There is good evidence for a peptide PIF as well. There are a number of prolactin-releasing factors (PRFs) which include oxytocin, vasoactive intestinal polypeptide, PHI and TRH. Several other peptides can also release prolactin, including angiotensin II. In response to stress there is a complex interaction of peptides intrahypothalamically. CRF augments its own release by an ultra short-loop positive feedback, and there is negative ultra short-loop feedback of GRF and somatostatin. Vasopressin appears to augment CRF release as well as to act directly on the pituitary, and there are complex interactions of various peptides to influence prolactin and GH release.
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PMID:The role of brain peptides in neuroimmunomodulation. 347 67

Corticotropin-releasing factor (CRF), a 41 amino acid polypeptide, has been isolated from ovine hypothalamic extracts, sequenced, and synthesized. It has a high potency for stimulating the secretion of corticotropin-like and beta-endorphin-like immunoactive substances in vitro and in vivo in laboratory animals and humans. The high concentration of CRF-like immunoactivity in hypophyseal portal plasma supports the hypothesis that CRF is the physiological hypothalamic factor. Human and rat CRF (rCRF) also have been purified and synthesized. They have an 83% sequence homology with ovine CRF (oCRF). oCRF-like activity has been found in human hypothalamus, pituitary stalk, posterior pituitary, thalamus, cerebral cortex, cerebellum, pons, medulla oblongata, spinal cord and in the adrenal, lung, liver, stomach, duodenum and pancreas. oCRF-like activity also has been found in the human placenta and in tissues producing ectopic ACTH. The action of CRF can be potentiated by vasopressin, oxytocin, epinephrine, norepinephrine, VIP, and angiotensin II. Intracerebroventricular administration of CRF in the rat produces prolonged elevations of plasma epinephrine, norepinephrine, glucose and glucagon; elevates mean arterial pressure and heart rate; increases motor activity and exploration in familiar surroundings and oxygen consumption; and decreases feeding and sexual behavior. Testing with CRF has enabled the separation of patients with hypothalamic and pituitary adrenal insufficiency. The CRF stimulation test has been useful in distinguishing pituitary from ectopic causes of Cushing's disease. The distribution of CRF within and beyond the hypothalamus provides an anatomical context for the observation that CRF can simultaneously activate and coordinate metabolic, circulatory and behavioral responses that are adaptative in 'stressful' situations. CRF not only stimulates the pituitary-adrenal axis in man, but it also influences several aspects of CNS function which may be of relevance to psychiatric illnesses.
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PMID:Corticotropin-releasing factor (CRF)--a review. 353 10

A possible involvement of oxytocin (OT) has been indicated in regulation of water and electrolyte metabolism, based on findings that the secretion of OT is increased by either water deprivation or sodium loading. However, to date, no informations have yet been obtained about the role of OT in hypertension. The present study was therefore undertaken to elucidate the role of OT for abnormalities of fluid and electrolyte metabolism in essential hypertension (EH) in comparison with normotensive subjects (NT). The major results were as follows. Plasma level of OT was 3.7 +/- 2.1 pg/ml (mean +/- SD) in EH, not significantly higher than that in NT (3.2 +/- 1.7 pg/ml). Plasma OT in low-renin EH (4.8 +/- 2.5 pg/ml) was significantly different from that in high-renin EH (2.9 +/- 1.4 pg/ml, p less than 0.05) and NT (p less than 0.05), but not in normal-renin EH (3.8 +/- 2.0 pg/ml). Plasma OT was inversely correlated with plasma renin activity (PRA) in EH (r = -0.384, p less than 0.01), but not in NT (r = 0.102). No significant correlation was found between plasma OT and plasma aldosterone concentration (PAC), plasma concentration of antidiuretic hormone (ADH), serum sodium and potassium, blood pressure and renal function in either EH or NT. I.m. injection of OT (0.04 IU/kg) increased significantly urinary excretions of sodium and potassium in EH and NT. However, the increment in sodium excretion was greater in low-renin EH than that in normal-renin EH (0.05 less than p less than 0.10), high-renin EH (p less than 0.05) and NT (p less than 0.05). PRA, PAC and ADH were significantly decreased after OT injection, but blood pressure, serum sodium and potassium were not altered in both EH and NT. I.v. administration of OT (0.1 approximately 0.2 IU/min) suppressed angiotensin II-induced increase of PAC and elevation of blood pressure in both EH and NT. The decrease in PAC by the OT administration was the greatest in low-renin EH. The reduction of blood pressure was significantly greater in EH than in NT (p less than 0.05). I.v. administration of hypertonic saline (5%) resulted in a significant increase of plasma OT in EH and NT, and the increment in OT was the greatest in low-renin EH. Serum sodium concentration was increased by the infusion, positively correlated with plasma OT in both EH (r = 0.458, p less than 0.05) and NT (r = 0.830, p less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Significance of oxytocin to disorders of fluid and electrolyte metabolism in patients with essential hypertension]. 356 5

Tissue specimens from various parts of the uteroplacental unit were obtained from women undergoing caesarean section, and placental tissue from women with normal deliveries. Strips of myometrial tissue, and segments of intramyometrial arteries were dissected together with segments of chorionic plate arteries and veins, and stem villous arteries. The preparations were mounted in organ baths, isometric tension recorded, and the responses to angiotensin II, vasopressin, and oxytocin were studied. In myometrial preparations, angiotensin caused a slight, transient increase in the frequency of spontaneous contractions, but no changes in amplitude. In all vascular preparations angiotensin produced concentration-related contractions. The responsiveness of the preparations was myometrial artery greater than villous artery greater than chorionic plate artery = chorionic plate vein. All responses were transient and tachyphylaxis was pronounced in all tissues. Tachyphylaxis was not influenced by pretreatment with indomethacin. Vasopressin increased transiently frequency and amplitude of contractions in myometrial strips. Myometrial arteries responded with a sustained contraction, as did chorionic plate arteries and veins but the latter vessels were less responsive. Villous arteries did not respond to vasopressin. Oxytocin preferentially stimulated myometrial strips, but also had a weak concentration-related contractant effect on chorionic plate arteries and veins. Villous arteries did not respond to oxytocin. At a higher concentration, causing a pronounced increase in the frequency and amplitude of contractions of myometrial strips, oxytocin abruptly caused a marked contraction of myometrial arteries. Lower concentrations of the peptide had almost no effects. The results suggest that various smooth muscle tissues of the human uterus and placenta are highly differentiated as regards responses to angiotensin II, vasopressin, and oxytocin. The physiological and possible clinical importance of the present findings deserve further investigation.
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PMID:Differential effects of angiotensin, vasopressin and oxytocin on various smooth muscle tissues within the human uteroplacental unit. 376 72

Extracellular single unit recordings were obtained to investigate the effects of systemic administration of angiotensin II (ANG II) on the excitability of antidromically identified neurohypophysial neurons in the rat. Records were obtained from 89 oxytocin- or vasopressin-secreting neurons in the hypothalamic supraoptic or paraventricular nuclei. Increased excitability in response to ANG II was observed in 83% of putative vasopressin- and 75% of putative oxytocin-secreting neurons tested in intact animals. Lesion studies to identify the central nervous system site of action for such peripherally administered ANG II showed that, after electrolytic lesion of the rostral subfornical organ (SFO), neurohypophysial neurons demonstrated no increase in excitability in response to this peptide. In an attempt to correlate the synaptic events through which activation of SFO neurons may result in facilitated excitability of neurohypophysial cells, 19 cells were tested with both systemic ANG II and electrical stimulation in the SFO. These studies demonstrated that all cells which showed long-duration increases in excitability in response to electrical stimulation of SFO were also activated by systemic ANG II. It is concluded that the SFO is an essential central nervous system structure in eliciting increases in the excitability of both oxytocin- and vasopressin-secreting neurons in response to systemic ANG II. These effects may involve the activation of SFO efferents that evoke long-duration post-synaptic changes in neurohypophysial cell excitability.
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PMID:Systemic angiotensin acts at subfornical organ to facilitate activity of neurohypophysial neurons. 376 70

The vasoconstrictor and vasopressor actions of vasopressin have been revealed in recent research through the use of highly specific and sensitive radioimmunoassays, employment of peptide antagonists, and comparison with an animal model which has hereditary absence of this hormone, the Brattleboro rat. Factors now known to modify the pressor effect of vasopressin are the baroreflexes, local vascular prostaglandin production, and a specific interaction with angiotensin II. In experimental models the volume retaining, but not the vasoconstrictor effect of vasopressin is necessary for mineralocorticoid-salt hypertension. Vasopressin contributes directly to the increase in arterial pressure of glycerol induced acute renal failure. In nephrectomized rats, plasma vasopressin is elevated and contributes directly to maintenance of pressure. Vasopressin antagonism may reduce arterial pressure in Goldblatt 1 and 2 kidney hypertension and in one genetic model, spontaneously hypertensive rat (SHR), but the peptide is not necessary for hypertension in these models. Plasma vasopressin is reduced in primary aldosteronism, but may be elevated in malignant hypertension. In essential hypertension, there is considerable disagreement among various studies in which plasma vasopressin, urine vasopressin excretion, platelet associated vasopressin, or vasopressin-neurophysin were measured as to whether there is evidence for increased secretion of vasopressin. Only preliminary studies of vasopressin antagonism in clinical hypertension have been reported. At present, there is no conclusive evidence that elevated vasopressin secretion occurs or is necessary for any form of clinical hypertension.
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PMID:The role of vasopressin in experimental and clinical hypertension. 388 2

Various agonists induced sustained contractions of estrogen-dominated rat uterine smooth muscle in Ca-free salt solution containing 0.2 mM EGTA after incubation of the muscle with 3 mM EGTA for 1 hr. The magnitudes of contraction varied with agonists. (bradykinin greater than oxytocin greater than or equal to vasopressin greater than PGF2 alpha greater than angiotensin II greater than acetylcholine greater than or equal to PGE2 greater than or equal to 5-hydroxytryptamine. Addition of 10(-4) Ca ion reduced the tension developed: Ca ion inhibited these contractions when they were sufficiently large (marked inhibition on bradykinin-, oxytocin-, and vasopressin-induced contractions; definite one on PGF2 alpha-induced contraction), as observed previously with oxytocin-induced contraction under the same conditions and named "Ca Reversal".
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PMID:Calcium reversal: inhibition by Ca ion of sustained contraction in Ca-free medium induced by various agonists in rat uterine smooth muscle. 392 49

A crude aqueous alcoholic extract of Mandevilla velutina (Apocynaceae) rhizomes produced a concentration-dependent displacement to the right of the concentration-response curve to bradykinin (Bk) in the isolated uterus of the rat. Schild analysis of the data revealed a linear relationship (r = 0.99) and yielded a pA2 value of 3.3 + 0.08 (- log g ml-1) but the slope differed significantly from unity. The anti-Bk action was of rapid onset and was reversible upon washout. Contractions induced by acetylcholine, oxytocin, angiotensin II and BaCl2 were unaffected by the extract. This represents the first report of a selective Bk antagonist of plant origin. The isolation of the active principle(s) may result in a useful pharmacological tool for elucidating the physiological and physiopathological roles of endogenous Bk.
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PMID:The selective antagonism of bradykinin action on rat isolated uterus by crude Mandevilla velutina extract. 404 75

Short-latency emetic responses were induced in dogs by injecting angiotensin II (AII), arginine vasopressin (AVP), and neurotensin (NTN) into cerebroventricular (ICV) and cisternal (ICT) sites also responsive to the emetic effects of apomorphine (APO). Angiotensin III, bradykinin, bombesin, oxytocin, adrenocorticotropic hormone, substance P, gastrin-related peptide and cholecystokinin were ineffective. The results suggest a possible dopaminergic mediation of peptide-induced emesis by receptors in the area postrema (AP).
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PMID:Emetic effects of centrally administered angiotensin II, arginine vasopressin and neurotensin in the dog. 404 79


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