Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various endocrine responses to 5-hydroxytryptamine (serotonin, 5-HT) agonists were used to assess serotonergic receptor function after chronic treatment with the antidepressants fluoxetine (10 mg/kg), a 5-HT uptake blocker and the norepinephrine uptake blocker desipramine (DMI, 5 mg/kg). Both were injected (i.p.) once a day for 21 days. DOI (5-HT1C/2 agonist, 0-5 mg/kg i.p.) and 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) (less selective, but predominantly a 5-HT1C agonist, 0-20 mg/kg i.p.) were administered 18 hr after the final antidepressant injection and 30 min before decapitation. Chronic treatment with both fluoxetine and DMI produced a potentiation in most hormone responses to the 5-HT agonists (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane HCl (DOI) and MK-212, although there were several differences in individual hormone responses to the two 5-HT agonists. Fluoxetine and DMI potentiated the MK-212- and DOI-induced increase of plasma oxytocin levels and potentiated the effect of DOI on plasma adrenocorticotropic hormone (corticotropin) and prolactin levels. In contrast, the effect of the high dose of MK-212 on plasma prolactin concentration was reduced by both antidepressants. Only MK-212 increased vasopressin levels and this effect was potentiated by fluoxetine, but not by DMI. Fluoxetine also significantly increased the resting level of plasma vasopressin. DMI potentiated the effect of MK-212 on plasma renin concentration. Pretreatment with fluoxetine significantly increased (38%) the Bmax for the 5-HT1C/2 agonist sites ([125I]DOI) in the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term treatment with the antidepressants fluoxetine and desipramine potentiates endocrine responses to the serotonin agonists 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) and (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI). 839 20

Holstein bull calves were used to examine the effect of dry feed on water balance and fecal moisture content during the suckling period. In Experiment 1 (n = 20 calves), free access to concentrate and timothy hay decreased urine volume and increased apparent water retention, fecal water excretion, and fecal moisture content by 2 wk, although daily amounts of milk replacer also affected water balance when DMI from dry feed was low. In Experiment 2 (n = 20 calves), free access to concentrate and hay from wk 1 increased reabsorption of water from renal tubules during wk 2, resulting in reduced urine volume and increased plasma volume. In Experiment 3 (n = 10 calves), supplementation of 500 g/d of milk replacer plus free access to concentrate and hay from wk 1 increased plasma antidiuretic hormone by 2 wk compared with the concentration in calves receiving 200 g/d of milk replacer alone. Plasma antidiuretic hormone concentrations were highly correlated with plasma concentrations of acetate and ketone bodies but not with glucose and urea. In Experiment 4 (n = 16 calves), apparent water retention and fecal moisture content during wk 2 were increased by free access to concentrate from wk 1 but were not affected by rice straw as an inert bulk source.
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PMID:Water balance and fecal moisture content in suckling calves as influenced by free access to dry feed. 1006 54

Twelve 18-mo-old Debouillet ewes were used to determine the effect of ruminal glucose infusion on DMI, on urinary ammonium (NH4+) and urea N (UUN) concentrations, and on serum metabolite and hormone profiles. Ewes were limit-fed a 90% concentrate diet for 30 d, stratified by BW into three groups (average BW = 82.6+/-1.1 kg), and assigned randomly to receive 0, 5, or 10 g of glucose/kg of BW via esophageal intubation. Urine was collected hourly for 12 h and blood (jugular venipuncture) at 30-min intervals for 12 h. After 12 h, ewes were housed individually, allowed free access to the diet, and DMI was recorded for 5 d. Venous blood pH averaged 7.49, 7.48, and 7.48 at 0 h and decreased (linear [L], P < .01) at 12 h (7.41, 7.36, and 7.26) with increasing glucose. Serum glucose increased (L, P = .06) at 3 and 6 h. Serum L(+)-lactate increased (L, P = .08) at 3, 6, and 9 h, whereas serum D(-)-lactate increased linearly (P = .09) at 6 and 9 h and quadratically (P < .10) at 12 h. After the glucose challenge, DMI decreased (L, P < .05). Urinary pH and NH4+ were not influenced by glucose infusion; however, UUN increased at 3 (quadratic [Q], P < .05), 4, 5, 6 (L, P = .03), and 7 h (Q, P < .05) and decreased at 11 and 12 h (L, P = .09). As glucose infusion increased, serum creatinine increased at 9 (L, P < .01) and 12 h (Q, P = .02). Generally, serum Na and P increased (P = .09), whereas K decreased (P < .05), with glucose infusion. Lactate dehydrogenase activity increased with glucose infusion (Q, P < .10) at 3, 6, 9, and 12 h. Increasing glucose infusion increased serum globulin (Q, P = .06), albumin, and total protein (L, P = .08). Serum prolactin and vasopressin were not influenced (P = .22) by glucose infusion. Serum insulin and aldosterone increased quadratically (P = .08), whereas serum growth hormone decreased linearly (P = .08) as a result of increasing glucose infusion. Results suggest that UUN, serum insulin, aldosterone, and several serum constituents may serve as markers of organic acid load in ruminants fed high-concentrate diets.
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PMID:Effect of ruminal glucose infusion on dry matter intake, urinary nitrogen composition, and serum metabolite and hormone profiles in Ewes. 1056 79