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M de Mello-Aires

Publications and source records attributed to M de Mello-Aires.

5 recordsLinked to original sources
PubMed1997

Luminal arginine vasopressin stimulates Na(+)-H+ exchange and H(+)-ATPase in cortical distal tubule via V1 receptor.

Bicarbonate reabsorption was evaluated by stationary microperfusion of in vivo early distal (ED) and late distal (LD) segments of rat kidney. Intratubular pH was recorded by double-barreled H ion-exchange resin/reference (1 M KCl) microelectrodes for the determination of HCO3- reabsorption. In the presence of luminal arginine vasopressin (AVP, 10(-9) M), a significant increase in HCO3- reabsorption was observed both in ED (from 0.931 +/- 0.061 to 2.12 +/- 0.171 nmol.cm-2.s-1] and LD segments [from 0.542 +/- 0.086 to 1.67 +/- 0.111 nmol.cm-2.s-1]. The addition of the V1-receptor antagonist [(d (CH2)5, Tyr (Et)2) arginine vasopressin] (10(-5) M) to luminal perfusion blocked luminal AVP mediated stimulation in ED and LD segments. 5-(N, N-hexamethylene) amiloride (10(-4) M) added to luminal perfusion inhibited luminal AVP-mediated stimulation in ED (by 63.7%) and LD (by 34.1%) segments. The addition of Bafilomycin A1 (2 x 10(-7) M) to the luminal perfusion did not affect luminal AVP-mediated stimulation in ED segments, but reduced it (by 31.7%) in LD segments. Our results indicate that luminal AVP acts to stimulate the Na(+)-H+ exchange in ED and LD segments via activation of V1 receptors, as well as the vacuolar H(+)-ATPase in LD segments.

Amiloride↗
PubMed1984

Proximal tubular HCO3-, H+ and fluid transport during maleate-induced acidification defect.

The mechanism of tubular acidification was studied in proximal tubular acidification defect induced in rats by acute parenteral infusion of maleate (200 mg/kg), which causes diuresis and bicarbonaturia. Proximal tubular bicarbonate reabsorption and H+ ion secretion were determined by stopped-flow microperfusion and measurement of luminal pH by Sb microelectrodes. Stationary pH increased in proximal tubule from 6.78 to 7.25 and bicarbonate reabsorption decreased from 1.32 to 0.51 nmol/cm2 X s. In these segments, mean cell PD fell from -66.6 to -20.2 mV, while Jv as estimated by the Gertz technique fell to 15% of controls. A similar impairment of acidification was observed during luminal and capillary perfusion with phosphate Ringer's. Since H+-ion efflux from the lumen was not significantly increased and both acidification and alkalinization half-times (t/2) were increased, no evidence for an increase in passive permeability for H+/HCO3- was obtained. The increased t/2 found during luminal perfusion with acid phosphate indicates, according to an electrical analog model, a reduction in pump series conductance. These results show that maleate affects both proximal Na+ and H+ transport; this effect may be ascribed to impairment of sodium-dependent transport systems in the brush-border membrane.

Acid-Base Equilibrium↗
PubMed1973

Kinetics of potassium transport across single distal tubules of rat kidney.

1. The transport of potassium across the distal tubular epithelium was studied in vivo in rats on a normal potassium intake and in rats in which distal tubular potassium secretion was either stimulated by potassium loading or the I.V. administration of a 5% sodium bicarbonate solution or in which potassium secretion was suppressed by dietary deprivation of potassium or sodium.2. (42)K was used to measure unidirectional fluxes across the luminal and peritubular cell membranes and to assess the magnitude of cellular potassium partaking in the transport process. This was accomplished by the simultaneous perfusion of the peritubular capillary network with (42)K-Ringer and of the distal tubular lumen with initially tracer-free solution. From the steady-state flux and the time course of tracer washout into the lumen after discontinuing the peritubular perfusion, unidirectional fluxes, rate coefficients of ion transfer and cellular transport pools could be measured.3. Transepithelial movement of potassium involves mixing with a variable cellular potassium transport pool. The latter is significantly elevated in conditions of enhanced distal tubular potassium secretion; cellular potassium labelling is reduced in conditions in which potassium secretion has been suppressed by potassium deprivation.4. Evidence is presented that changes in the peritubular transport pattern are primarily responsible for modifications of potassium translocation. Thus, stimulation of potassium secretion is associated with increased peritubular potassium uptake; a reduced potassium uptake across the peritubular cell membrane accounts for the fall in potassium secretion in potassium-depleted animals. Whereas passive entry of potassium across the peritubular membrane is augmented in potassium-loaded animals, the induction of metabolic alkalosis by the administration of 5% sodium bicarbonate stimulates active potassium uptake across the peritubular cell membrane. Sodium deprivation stimulates active reabsorptive transfer of potassium from the tubular lumen.

Alkalosis↗