Kouritas V K, Hatzoglou C H, Gourgoulianis K I, Molyvdas P A
Department of Physiology, Medical School of Larissa, University of Thessaly, Greece.
Exp Clin Endocrinol Diabetes. 2010 May;118(5):328-32. doi: 10.1055/s-0030-1247543. Epub 2010 Feb 16.
Insulin induces electrochemical alterations in sheep visceral and parietal pleura, an effect abolished by the Na (+)-channel blocker amiloride and the Na (+)-K (+) pump inhibitor ouabain. The aim of this study was to further investigate the role of different electrolytes and glucose in these electrochemical changes.
Sheep pleural specimens were mounted in Ussing chambers. Insulin (10 (-7)M) was added mesothelially in Na (+), K (+), Ca (2+)-free, low H (+) and glucose solutions. In other experiments, specimens were pretreated with K (+) and Ca (2+)-free Krebs solutions. Trans-mesothelial Resistance was determined.
Insulin did not increase Trans-mesothelial Resistance of visceral and parietal pleura in K (+)-free (p=0.008 and p=0.028 respectively), Ca (2+)-free (p=0.006 and p=0.012 respectively) and low glucose (p=0.009 and p=0.03 respectively) solutions. This effect was totally inhibited in Na (+)-free solutions or in specimens pretreated with Ca (2+) -free Krebs solution and partially inhibited, when low H (+) solutions were used (p=0.042 for visceral and p=0.045 for parietal).
Insulin-induced electrochemical changes in sheep pleura are mainly associated with alterations in Na (+) and Ca (2+) concentrations. Since amiloride and ouabain abolish these electrochemical changes, it may be suggested that insulin could influence the pleural fluid recycling, mainly via the Na (+) transportation system, irrespective of the glucose content.