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Am J Physiol Renal Physiol 280: F239-F243, 2001;
0363-6127/01 $5.00
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Vol. 280, Issue 2, F239-F243, February 2001

Peritubular fluid viscosity modulates H+ flux in proximal tubules through NO release

Paula Díaz-Sylvester1,2, Myriam Mac Laughlin1, and Carlos Amorena1,2

1 Instituto de Investigaciones Cardiológicas-Consejo Nacional de Investigaciones Científicas y Técnicas, 1122 Buenos Aires; and 2 Escuela de Ciencia y Tecnología, Universidad Nacional de General San Martín, 1650 San Martín, Argentina

We evaluated the effects of increasing the viscosity (eta ) in peritubular capillary perfusates (PCP; 20 mM HNaPO4--Ringer, pH 7.4) on proximal convoluted tubule (PCT) acidification. Micropuncture experiments were performed with simultaneous luminal and peritubular perfusion. Changes in pH of a 20 mM HNaPO4--Ringer (pH 7.4 at t = 0) droplet placed in PCT lumen were measured with H+-sensitive microelectrodes. By adding neutral dextran (molecular wt 300,000-400,000) to the PCP, eta  was increased. The effect of 10-5 M ATP added to normal-eta PCP was evaluated. High eta  increased H+ flux (85 and 97% when eta  was increased 20 and 30%, respectively, above the control value). This increase was abolished by adding the nitric oxide antagonist Nomega -nitro-L-arginine (L-NNA; 10-4 M) or the purinoreceptor antagonists suramin (10-4 M) and reactive blue 2 (3 × 10-5 M). Addition of 5 × 10-3 M L-arginine to the peritubular perfusate overcame the inhibitory effect of L-NNA on high-eta -induced increase in H+ flux. ATP increased H+ flux (80%), and this effect was blocked by L-NNA. These results suggest that changes in eta  can modulate proximal H+ flux, at least in part, through ATP-dependent nitric oxide release from the endothelial cells of the peritubular capillaries.

nitric oxide; shear stress; adenosine 5'-triphosphate antagonists; Nomega -nitro-L-arginine; micropuncture; hydrogen ion secretion


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