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Effect of uroguanylin on potassium and bicarbonate transport in rat renal tubules

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The effect of uroguanylin (UGN) on K+ and H+ secretion in the renal tubules of the rat kidney was studied using in vivo stationary microperfusion. For the study of K+ secretion, a tubule was punctured to inject a column of FDC-green-colored Ringer's solution with 0.5mmol KCl/L ± 10−6 mol UGN/L, and oil was used to block fluid flow. K+ activity and transepithelial potential differences (PD) were measured with double microelectrodes (K+ ion-selective resin vs. reference) in the distal tubules of the same nephron. During perfusion, K+ activity rose exponentially, from 0.5mmol/L to stationary concentration, allowing for the calculation of K+ secretion (JK). JK increased from 0.63 ± 0.06 nmol·cm–2·s–1 in the control group to 0.85 ± 0.06 in the UGN group (p < 0.01). PD was –51.0 ± 5.3 mV in the control group and –50.3 ± 4.98 mV in the UGN group. In the presence of 10−7 mol iberiotoxin/L, the UGN effect was abolished: JK was 0.37 ± 0.038 nmol·cm–2·s–1 in the absence of, and 0.38 ± 0.025 in the presence of, UGN, indicating its action on maxi-K channels. In another series of experiments, renal tubule acidification was studied, using a similar method: proximal and distal tubules were perfused with solutions containing 25mmol NaHCO3/L. Acidification half-time was increased both in proximal and distal segments and, as a consequence, bicarbonate reabsorption decreased in the presence of UGN (in proximal tubules, from 2.40 ± 0.26 to 1.56 ± 0.21 nmol·cm–2·s–1). When the Na+/H+ exchanger was inhibited by 10−4 mol hexamethylene amiloride (HMA)/L, the control and UGN groups were not significantly different. In the late distal tubule, after HMA, UGN significantly reduced JHCO3, indicating an effect of UGN on H+-ATPase. These data show that UGN stimulated JK+ by acting on maxi-K channels, and decreased JHCO3 by acting on NHE3 in proximal and H+-ATPase in distal tubules.

On a examiné l’effet de l’uroguanyline (UGN) sur la sécrétion de K+ et de H+ dans les tubules rénaux de rats en utilisant la technique de microperfusion stationnaire in vivo. Pour examiner la sécrétion de K+, on a perforé un tubule pour injecter 0,5mmol/L de KCl ± 10−6 mol/L d’UGN dans une colonne de solution de Ringer colorée au FDC-vert, et utilisé de l’huile pour bloquer l’écoulement du liquide. On a mesuré l’activité K+ et la DP transépithéliale au moyen de deux microélectrodes (résine sélective aux ions K+ vs. référence) implantées dans le tubule distal du même néphron. Durant la perfusion, l’activité K+ a augmenté expontiellement de 0,5mmol/L jusqu’à une concentration stationnaire (Ks) permettant de mesurer la sécrétion de K+ (JK). La JK a augmenté de 0,63 ± 0,06 nmol·cm–2·s–1 durant la perfusion témoin à 0,85 ± 0,06 durant l’UGN, p < 0,01. La DP a été de –51 ± 5,3 mV durant la perfusion témoin et de –50,3 ± 4,98 mV durant l’UGN. En présence de 10−7 mol/L d’ibériotoxine, l’effet de l’UGN a été supprimé : la JK a été de 0,37 ± 0,038 nmol·cm–2·s–1 en l’absence d’UGN et de 0,38 ± 0,025 en présence d’UGN, ce qui démontre son action sur les canaux maxi-K. Dans une autre série d’expériences, on a examiné l’acidification du tubule rénal par une méthode similaire, en perfusant les tubules proximal et distal avec des solutions contenant 25mmol/L de NaHCO3. La demi-vie de l’acidification a augmenté dans les segments proximal et distal; par conséquent, la réabsorption de bicarbonate a été diminuée par l’UGN (dans les tubules proximaux, de 2,40 ± 0,26 à 1,56 ± 0,21 nmol·cm–2·s–1). Lorsqu’on a inhibé l’échangeur Na+/H+ au moyen de 10−4 mol/L d’hexaméthylène amiloride (HMA), la perfusion témoin et l’UGN ont eu des effets quasi similaires. Dans la partie terminale du tubule distal, l’UGN a nettement réduit la JHCO3 après l’administration de la HMA, ce qui démontre un effet de l’UGN sur la H+-ATPase. Ces résultats indiquent que l’UGN a stimulé la JK+ en agissant sur les canaux maxi-K et diminué la JHCO3 en agissant sur NHE3 dans le tubule proximal et sur H+-ATPase dans le tubule distal.

Document Type: Research Article

Publication date: 2006-10-01

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