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dc.contributor.author De Châtel, Rudolf
dc.contributor.author Barna, István
dc.contributor.author Tóth, Miklós
dc.contributor.author Gyertyanfy G
dc.contributor.author Krasznai I
dc.date.accessioned 2016-10-12T12:47:44Z
dc.date.available 2016-10-12T12:47:44Z
dc.date.issued 1991
dc.identifier 0026068026
dc.identifier.citation pagination=95-101; journalVolume=77; journalIssueNumber=2; journalTitle=ACTA PHYSIOLOGICA HUNGARICA;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/3736
dc.description.abstract The renal prostaglandins are involved in the regulation of sodium balance. In the present study exchangeable body sodium (NaE) and the urinary excretion of the stable metabolite of prostacyclin, 6-keto-prostaglandin F1 alpha (6-k-PGF1 alpha) were determined simultaneously in 10 hospitalized healthy individuals. NaE was 1461 +/- 107 mmol/m2 body surface area, or 98.5 +/- 6.9% when expressed as percent of the normal value assessed on the basis of measurements in 54 control subjects. The excretion of 6-k-PGF1 alpha amounted to 68.3 +/- 39.2 ng/4 hr. Statistical evaluation revealed significant correlation between NaE and PGF1 alpha excretion (r = 0.642; p less than 0.05) and between the serum Na concentration and the urinary excretion of 6-k-PGF1 alpha (r = 0.865; p less than 0.001). The obtained results indicate that urinary 6-k-PGF1 alpha excretion, hence the renal synthesis of prostacyclin, are regulated, among other factors, by body sodium stores. The increased production of prostacyclin with expanding sodium space might be regarded as a compensatory response contributing to the renal elimination of excess sodium from the body. The signal to this response could be the serum Na concentration.
dc.relation.ispartof urn:issn:0231-424X
dc.title Relationship between exchangeable body sodium and urinary 6-keto-prostaglandin F1 alpha excretion in normal man.
dc.type Journal Article
dc.date.updated 2016-10-10T14:03:26Z
dc.language.rfc3066 en
dc.identifier.mtmt 1593249
dc.identifier.wos A1991GD12700001
dc.identifier.pubmed 1927543
dc.contributor.department SE/AOK/K/I. Sz. Belgyógyászati Klinika
dc.contributor.institution Semmelweis Egyetem


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