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

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Artigo
Data de publicação
2006
Periódico
Canadian Journal of Physiology and Pharmacology
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17
Autores
Amorim J.B.O.
Musa-Aziz R.
Lessa L.M.A.
Malnic G.
Fonteles M.C.
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Resumo
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 0.5 mmol 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 0.5 mmol/L to stationary concentration, allowing for the calculation of K+ secretion (J K). 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: J K 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 25 mmol NaHCO 3/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. © 2006 NRC.
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