Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In pharmacological doses dopamine (DA) will interact with several endocrine systems and both inhibit (prolactin, thyrotropin) and enhance (renin, angiotensin) hormonal release. In this study we have examined whether DA given to preterm neonates will influence prostaglandin (PG) production. The question is of importance since vasodilator PGs play a role in postnatal adaptation. We determined the effect of low dose DA infusion on the 24 h urinary PGE2 excretion rate (an index of renal PGE2 synthesis) in preterm infants. Six preterm neonates, with a 24-h requirement of 2 micrograms/kg per min DA treatment for oedema, moderate oliguria, poor peripheral perfusion and/or mild systemic hypotension were studied on days 2 (Day 1), 3 (Day 2, the day of DA infusion), and 4 (Day 3, DA discontinued) of life. Six preterm infants (control group) that did not require DA infusion were also studied to monitor possible spontaneous changes in the renal PGE2 production on days 2, 3 and 4 of life. In the control group urine output (Uv) and PGE2 excretion rate remained unchanged during the study. In the study group DA administration resulted in nearly two-fold increases in both the Uv (194%) and PGE2 excretion (182%). Urinary PGE2 excretion was, however, closely related to urine flow in both the control infants (Day 1-3) and the study group infants (Day 1-2). Since increased diuresis stimulates renal PGE2 production, our data suggest that the increased PGE2 excretion on Day 2 in the study group was not due to a direct effect of DA on PGE2 synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of low-dose dopamine infusion on urinary prostaglandin E2 excretion in sick, preterm infants. 318 Dec 3

A strong inverse relationship was found between the excretion rates of the prostaglandins PGE2 and PGF2 alpha and urine flow (and osmolar excretion rate) over a range of urine flow rates from 1.5 to 40 microliters . min-1 . g kidney weight-1, covering spontaneous variations and isotonic saline diuresis. These results suggest the operation of a negative feedback mechanism by which the diuretic action of the prostaglandins, as part of a defence system, counteracts excessive oliguria. PGE2 excretion did not correlate with either urinary kallikrein excretion or plasma renin concentration. When the concentrating mechanism was interfered with by reducing renal perfusion pressure to, or below 65 mmHg, and vasopressin was given i.v. PGE2 excretion rate roughly parallelled urine--and probably medullary interstitial osmolar activity. However, in hydropenic rats there was no correlation between urine osmolality (Uosm) and PGE2 excretion over a range of osmolalities from 500 to 2 500 mOsm . kg-1, nor any relationship between delta Uosm and delta PGE2 excretion. Thus, a high interstitial osmolar activity appears to be a prerequisite for the activation of PG-synthesis in the renal medulla, but another (other) yet undefined factor(s) play the major role as (a) determinant(s) for PG-excretion in vivo.
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PMID:On the relationship between urinary PGE2 and PGF2 alpha excretion rates and urine flow, osmolar excretion rate and urinary osmolality in anesthetized rats. 695 76

To examine the role of prostaglandins and the kallikrein system in the recovery from acute renal failure, we studied the sequential changes in urinary prostaglandins and kallikrein after the onset of oliguria. The six patients studied had acute tubular necrosis of the vasomotor type. Urinary PGE2, PGF2 alpha, the PGF2 alpha-main urinary metabolite, 6-keto-PGF1 alpha and TXB2 were all measured by radioimmunoassay. Urinary kallikrein was assayed by means of hydrolytic activity using a chromogenic tripeptide substrate. Following onset of diuresis, urinary PGE2 excretion was increased to normal, parallel to the increase in urine volume. In contrast, the ratio of urinary PGF2 alpha/PGE2 peaked at the onset of diuresis, indicating a relative increase in PGF2 alpha production at this time. Prior to this peak, urinary kallikrein concentrations reached the highest levels, suggesting a close connection with renal prostaglandin metabolism. On the other hand, changes in PGF2 alpha-MUM, 6-keto-PGF1 alpha and TXB2 were not found. These results indicate that there may be an interlocking acute alteration of the kallikrein-prostaglandin system occurring immediately before the resolution of oliguria, although the role of the acute shift to PGF2 alpha production observed needs further study.
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PMID:Urinary prostaglandins and kallikrein in the course of acute renal failure. 696 Mar 68