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. Recently it has been shown that injection of angiotensin II into the anterior diencephalon causes the rat to drink water. In the present experiments the dipsogenic action of a number of other substances including substances related to angiotensin was tested.2. Injection of 0.001 Goldblatt u. renin into the angiotensin-sensitive region causes the water-replete rat to drink. Drinking is slower in onset and continues for longer than after injection of angiotensin II.3. Synthetic tetradecapeptide renin substrate and angiotensin I were as effective as angiotensin II at causing water-replete rats to drink.4. beta-aspartic acid(1)-valine(5)-angiotensin II was also fully effective; but the D-arginine substituted octapeptide was much less effective.5. The (2-8) heptapeptide retained about 50% of the dipsogenic activity of the octapeptide, whereas the absence of phenylalanine at the other end of the peptide chain in the (1-7) heptapeptide results in an inactive compound.6. The (3-8) hexapeptide and the (4-8) pentapeptide, both of which have phenylalanine at the end of the chain, and the (1-4) and (5-8) tetrapeptide fragments of angiotensin II showed only a slight action on intake of water.7. Kallikrein, bradykinin, adenosine-3'5-cyclic phosphate, vasopressin and oxytocin caused no drinking when injected into the angiotensin-sensitive region.8. It is concluded that the requirements for the dipsogenic activity of angiotensin are the same as those for its other biological actions with the qualification that the precursor peptides are also active, presumably because they give rise to angiotensin II locally.
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PMID:The effect on drinking of peptide precursors and of shorter chain peptide fragments of angiotensin II injected into the rat's diencephalon. 432 62

A group of 89 individuals with essential hypertension was evaluated with several measurements including the neurophysin believed to be the human oxytocin neurophysin (OT-Np), and the human vasopressin neurophysin (VP-Np). The neurophysins are proteins synthesized within cells of the supraoptic and paraventricular nuclei in conjunction with their respective hormones oxytocin and vasopressin as part of a common precursor molecule and so may reflect the simultaneous presence in plasma of their associated hormones. A poor but statistically significant correlation was noted between levels of OT-Np and renin activity in plasma (PRA) either supine (r = 0.248) or erect (r = 0.255). Levels of OT-Np averaged 1.75 ng/ml and were inversely correlated with creatinine (r = -0.252), supine blood pressure (r = -0.450), plasma volume (r = -0.327), and 24-hour urine sodium (r = -0.313). Levels of Ot-Np could be suppressed by infusion of physiologic saline. Levels of OT-Np were lower in the volume expanded state and were positively correlated with the quantity of sodium excreted into a 24-hour urine collected after the infusion (r = 0.426) and inversely correlated with the supine systolic (r = -0.379) and supine diastolic (r = -0.455) blood pressures recorded after the infusion of saline. Oestrogen, a stimulus to the secretion of OT-Np, did not account for the elevation of OT-Np observed in the study, since mean levels of oestradiol (E2) in a subset of the patients with elevated OT-Np (E2 = 36 pg/ml) were not different from levels in subjects with lower values of OT-Np (E2 = 45 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Levels of the oxytocin-associated and vasopressin-associated neurophysins in plasma and their responses in essential hypertension. 637 63

Infusion of oxytocin into one vertebral artery of anesthetized dogs did not alter plasma vasopressin concentration, blood pressure or heart rate. However, there was a significant (p less than 0.01) increase in plasma renin activity (PRA; delta = 7.6 +/- 2.3 ng/ml X h). A 35% hemorrhage caused blood pressure to fall by 9.4 +/- 4.0 mm Hg (p less than 0.01) and PRA to rise by 8.8 +/- 2.7 ng/ml X h (p less than 0.05). In 8 dogs that were subjected to a similar hemorrhage and that also received an intravertebral infusion of oxytocin, blood pressure was maintained and PRA increased by 14 +/- 4.3 ng/ml X h (p less than 0.05). Heart rate and plasma vasopressin responses were similar in both hemorrhage groups. The results indicate that oxytocin prevented the fall in blood pressure associated with a hemorrhage, possibly by increasing renin release.
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PMID:Effect of vertebral artery infusions of oxytocin on plasma vasopressin concentration, plasma renin activity, blood pressure and heart rate and their responses to hemorrhage. 637 92

The effect of intense muscular work (80% of maximal oxygen uptake) on responses of plasma hormones involved in electrolyte and water balance were measured in 14 male subjects. They were divided into three groups according to their maximal oxygen uptake and the duration of exercise performed until exhaustion: well trained subjects (group I), trained subjects (group II), and untrained subjects (group III). Pulmonary gas exchange, heart rate, rectal and skin temperature, and weight loss were measured as well as hematocrit and plasma and urine sodium and potassium concentrations. Rectal temperature increased significantly in all subjects after exhaustion. The variation of hematocrit was smallest and the weight loss greatest in the well-trained subjects. Plasma aldosterone, renin activity (PRA), vasopressin (AVP), and neurophysin (Np) displayed highly significant increases after exercise in all three groups: PRA was increased 4.5 times (p < 0.01), aldosterone 13 times (p < 0.05), Np 2.6 times (p pe 0.05), and AVP 4.8 times (p < 0.05). Nevertheless, there was no correlation between the changes in PRA and those in plasma aldosterone, nor between aldosterone and plasma sodium or potassium. At the urinary level, the only striking observation was that free water clearance tends to become positive after exercise. Our results provide evidence that this kind of exercise produces a highly significant increase in plasma levels of the hormones involved in electrolyte and water balance. They also indicate that it is among the well-trained subjects that sweat loss is highest though the hematocrit increase is the smallest; this suggests that water is shifted more efficiently from the extravascular compartment.
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PMID:Plasma AVP, neurophysin, renin activity, and aldosterone during submaximal exercise performed until exhaustion in trained and untrained men. 699 37

Antihypertensive and general pharmacological properties of 1-[2-(1,3-dimethyl-2-butenylidene)hydrazino]phthalazine (budralazine) were studied in comparison with those of hydralazine. Single oral administration of budralazine (4--15 mg/kg) to DOCA/saline hypertensive rats resulted in a dose-related and sustained antihypertensive effect which was 2--3 times less potent than that of hydralazine. However, there were no remarkable differences between both drugs in the hypotensive magnitude after the 4-week treatment of spontaneously hypertensive rats (SHR) with their higher doses. After single oral administration, budralazine was about 8 times less potent than hydralazine in increasing plasma renin activity in normotensive rats. At effective antihypertensive doses, budralazine inhibited spontaneous motor activity (mice), gastrointestinal propulsion (mice), gastric emptying rate (rats), gastric secretion (rats), urine output and urinary electrolyte excretion (rats) as well as carrageenan-induced paw edema formation (rats), which were essentially less potent than those produced by hydralazine. Budralazine at 6 mg/kg i.v. exhibited a slowing of neocortical EEG (cats) and a slight increase in spinal monosynaptic potentials (cats) and inhibited gastrointestinal motility (dogs). The same dose of hydralazine produced an increase in occurrence of the neocortical fast waves, an inhibition of the monosynaptic potentials and the carotid sinus reflex (dogs) and a stimulation of intestinal motility followed by prolonged and marked reduction. Budralazine (10(-5) g/ml) slightly potentiated contractile response of isolated guinea-pig vas deferens to noradrenaline, whereas hydralazine (10(-4) g/ml) inhibited the response. Budralazine (10(-5) g/ml), like hydralazine (10(-4) g/ml), produced a nonspecific antagonism against the contractile response of isolated guinea-pig ileum to various spasmogens, and both drugs (10(-4) g/ml) reduced either spontaneous motility or oxytocin-induced motility in isolated rat uterus.
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PMID:Antihypertensive and general pharmacological properties of budralazine. 702 95

The role of suckling, prolactin, and gonadal steroids in regulating hypothalamic oxytocin (OT) mRNA content during the 1st and 2nd wk of lactation was evaluated. On day 4 of lactation, OT mRNA content decreased in rats removed from their litter for 24 h compared with suckled controls. Either suckling (in the absence of prolactin release) or prolactin (in the absence of suckling) maintained OT mRNA content at this stage of lactation. In contrast, at day 11 of lactation, OT mRNA content remained unchanged in rats deprived of pups for 24 h. Ovariectomy did not compromise the ability of day 11 nonsuckled rats to maintain OT mRNA content; however, the increased water intake, plasma prolactin, plasma vasopressin (VP), plasma renin concentration, and hypothalamic VP mRNA content at day 11 compared with day 4 suggest a role for fluid balance in determining OT mRNA content during the 2nd wk of lactation. Thus, at day 4, suckling is a major determinant of OT mRNA content as a result of both direct activation of neuronal afferents to the OT neurons and stimulation of prolactin release. This is in contrast to day 11, when fluid balance may predominate in regulation of OT mRNA.
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PMID:Role of prolactin and gonadal steroids in regulation of oxytocin mRNA during lactation. 763 81

Simultaneous administration of the diuretic furosemide (10 mg/kg) and a low dose of the angiotensin-converting enzyme (ACE) inhibitor captopril (5 mg/kg) results in short-latency thirst and sodium appetite (i.e., the rapid ingestion of water and NaCl solution). To elucidate potential mechanisms for mediating this behavior, changes in plasma levels of key hormones involved in fluid intake and balance were characterized in rats subjected to this treatment protocol. Rats treated jointly with furosemide and low-dose captopril had exaggerated increases in plasma renin activity and angiotensin I but equivalent increases in plasma aldosterone compared with rats treated with either agent alone. Treatment with furosemide plus low-dose captopril increased plasma vasopressin but not plasma oxytocin. The administration of a higher dose of captopril (100 mg/kg) with furosemide, a combination of drugs that does not stimulate fluid intake (29), further increased plasma renin activity and angiotensin I but prevented the rise in plasma vasopressin. The results support the hypothesis that thirst and salt appetite generated by this protocol depend on angiotensin II formed within brain circumventricular organs rather than the systemic circulation.
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PMID:Endocrine changes associated with a rapidly developing sodium appetite in rats. 797 42

The present study had two objectives: (1) to provide information on neuroendocrine challenge tests that can lead to diagnostic tests in humans; and (2) to confirm our previous observation that chronic fluoxetine selectively inhibits serotonin (5-HT1A) receptor function. We determined the effect of chronic fluoxetine and desipramine (DMI) on the hormone response to ipsapirone, a 5-HT1A agonist and a potential anxiolytic drug. Ipsapirone increased oxytocin, adrenocorticotropic hormone (ACTH), corticosterone, and prolactin, but not renin or vasopressin concentrations in plasma. Chronic fluoxetine, but not DMI, significantly inhibited the effect of ipsapirone on plasma oxytocin, ACTH and corticosterone concentrations. Chronic fluoxetine also reduced the Bmax for 3H-8-hydroxy-2-(dipropylamino) tetralin (3H-8-OH-DPAT) labelled 5-HT1A receptors in the midbrain. Neither antidepressant altered the density or affinity of 5-HT uptake sites. In conclusion, the present results confirm our previous results using 8-OH-DPAT as a challenge, and suggest that chronic 5-HT uptake inhibition results in adaptive changes leading to decreased function of the 5-HT1A receptor system. Finally, because ipsapirone may be administered to humans, it might be usable to evaluate 5-HT1A receptor function in depressed patients.
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PMID:Attenuation of hormone responses to the 5-HT1A agonist ipsapirone by long-term treatment with fluoxetine, but not desipramine, in male rats. 799 56

The present studies determined whether serotonin 5-HT1A receptor-mediated function is modified by chronic exposure to antidepressants. Hormone responses to the 5-HT1A agonist, 8-OH-DPAT, were evaluated after long-term exposure to two antidepressants, the 5-HT uptake blocker, fluoxetine, and the norepinephrine uptake blocker, desipramine (DMI). In addition, the density and affinity of 5-HT1A receptors in the hypothalamus and cerebral cortex were measured. Male rats received fluoxetine (10 mg/kg i.p.), DMI (5 mg/kg i.p.) or saline injections once daily for 21 days. 8-OH-DPAT (0-500 micrograms/kg s.c.) was administered 18 h after the final antidepressant injection and 15 min before sacrifice. 8-OH-DPAT significantly increased plasma ACTH, corticosterone, oxytocin and prolactin, but not renin or vasopressin concentrations. Chronic injections of fluoxetine inhibited the ACTH, corticosterone and oxytocin responses to 8-OH-DPAT, suggesting reduced 5-HT1A receptor function. In contrast, chronic DMI did not alter the hormone responses to 8-OH-DPAT. The density and affinity of 5-HT1A receptors in the frontal cortex or hypothalamus were not altered by either fluoxetine or DMI. To verify that the observed effects require prolonged exposure to fluoxetine, rats received a single injection of fluoxetine (10 mg/kg, i.p.), 3 h before 8-OH-DPAT (0-500 micrograms/kg s.c.). Acute fluoxetine did not reduce any of the hormone responses to 8-OH-DPAT. In conclusion, the results suggest that chronic, but not acute, exposure to fluoxetine decreases 5-HT1A receptor function. This effect is not seen in rats chronically exposed to DMI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term fluoxetine, but not desipramine, inhibits the ACTH and oxytocin responses to the 5-HT1A agonist, 8-OH-DPAT, in male rats. 811 81

Dietary NaCl deprivation stimulates a robust salt appetite in Wistar rats but has little influence on this behavior in rats of the Fischer 344 (F344) strain. To examine physiological substrates of attenuated salt appetite in F344 rats, several pertinent measures of renal function and fluid homeostasis were made in Wistar and F344 rats eating normal and NaCl-deplete diets. Physiological adjustments to NaCl deprivation were similar between the two strains; however, F344 rats showed smaller increases in plasma renin activity (PRA) than their Wistar counterparts. In addition, F344s decreased urinary sodium excretion more rapidly than Wistar rats in response to deprivation. The present studies also revealed several strain differences in baseline fluid and electrolyte regulation. Relative to the Wistar strain, F344 rats were characterized by high baseline PRA, increased arginine vasopressin (AVP) excretion, decreased urine volume, and diminished thirst. We propose that AVP and oxytocin activation may reduce salt preference and suppress the development of salt appetite in F344 rats.
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PMID:Physiological correlates of attenuated salt appetite in Fischer 344 rats. 814 Jan 78


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