Effect of an Acute Oral Ibuprofen Intake on Urinary Aquaporin-2 Excretion in Healthy Humans
|Title:||Effect of an Acute Oral Ibuprofen Intake on Urinary Aquaporin-2 Excretion in Healthy Humans|
|Authors:||Pedersen, Robert Schou; Bentzen, Hans; Bech, Jesper Norgaard; Pedersen, Erling Bjerregaard|
|Publisher:||Scandinavian Journal of Clinical and Laboratory Investigation|
|Date Published:||January 01, 2001|
This translation by the NDI Foundation is to assist the lay reader. To provide a clear, accessible interpretation of the original article, we eliminated or simplified some technical detail and complicated scientific language. We concentrated our translation on those aspects of the article dealing directly with NDI. The NDI Foundation thanks the researchers for their work toward understanding and more effectively treating this disorder.
© Copyright NDI Foundation 2007 (JC)
- urinary excretion of aquaporin-2 (u-AQP2),
- the amount of AVP in the blood, and
- the concentration of naturally occurring particles in the blood and urine.
The researchers hypothesized that the reduction of PG due to ibuprofen interferes with AVP action on collecting duct cells because a reduction in PG would result in an increase in AQP2. This increase would be reflected in an increase in the amount of AQP2 excreted in the urine by those subjects ingesting ibuprofen.
The researchers divided 15 healthy human volunteers into three groups. One group was given placebos, another 600 mgs of ibuprofen, and the last 1200 mgs. Both placebo and ibuprofen were given in two doses. Measurements on 12 of the subjects (3 subjects had to be excluded) showed the u-AQP2 increased in the ibuprofen groups and decreased in the placebo group. However, urinary output increased and urine concentrations decreased in all three groups. There was a slight increase in AVP in the placebo group and the 600 mg group, but not in the 1200 mg group. The researchers determined that the changes in u-AQP2 were not related to the changes in AVP, urinary output or the relative concentration of the urine.
It might be expected that the greater abundance of AQP2s that occurs when PG formation is inhibited by ibuprofen would result in a decrease in urinary output and a more concentrated urine. The researchers suggest that this did not occur either because the AQP2 increase is too discrete, or the ratio of AQP2 shed in the urine is greater than the normal rate. They suggest that the increased u-AQP2 indicates the ibuprofen has a direct effect on the collecting ducts.