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M de Mello Aires

Publications and source records attributed to M de Mello Aires.

6 recordsLinked to original sources

Filtered load of buffer and renal H-ion secretion: mechanism of proximal tubule load dependence.

When the filtered load of buffers like bicarbonate or phosphate is increased by elevating GFR or buffer concentration in plasma, the overall renal reabsorption of bicarbonate or the formation of titratable acidity are markedly increased. The same happens when buffer concentration or flow rate are varied during proximal microperfusion. We have recently studied the mechanisms of this functional dependence. We have observed that the rate of bicarbonate reabsorption is always proportional to luminal buffer concentration when a stationary fluid column is injected into the proximal lumen. H-ion secretion is also proportional to luminal levels of non-bicarbonate buffers. Using a pH-stat technique adapted to renal tubules, we have shown that H-ion secretion is dependent on proximal pH independently of the used buffer species. A kinetic analysis of these data shows a non-linear relationship between luminal H+ and H+ secretion, compatible with carrier mediated transport.

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Verapamil effect on renal function of normotensive and hypertensive rats.

The effect of verapamil, a Ca++ antagonist drug, on renal function and proximal fluid reabsorption in normal and hypertensive (GII) rats was studied. During intravenous infusion of verapamil, mean arterial pressure (MAP) fell significantly in both groups, 23% more in hypertensive than in normotensive rats. Glomerular filtration rate (GFR) was significantly higher in hypertensive rats and also increased significantly in this group during verapamil infusion. Effective renal plasma flow (ERPF) was similar in both groups and did not change significantly during verapamil infusion. The increase in urine flow, Na+ and Ca++ excretion was higher in hypertensive than in normotensive rats during verapamil infusion. When 10(-5) M verapamil was added to the luminal perfusate of proximal tubules, fluid reabsorption was reduced to 64% in normotensive and to 42% in hypertensive rats. When added to capillary perfusate, fluid reabsorption was almost completely but reversibly inhibited (92% in normotensive and 83% in hypertensive rats). Our findings indicate a direct effect of verapamil on renal Na+ and possibly also on Ca++ reabsorption, suggesting involvement of the Na+-Ca++ countertransport system. The greater effect of verapamil on Na+ excretion in hypertensive rats was not due to increased action on proximal Na+ reabsorption.

Absorption↗

Role of luminal buffers in renal tubular acidification.

The acidification of kinetics of artificial solutions containing buffers of different permeancy were studied in rat proximal tubules by means of stationary microperfusion techniques. Luminal pH changes were measured by antimony microelectrodes and used to calculate net rates of acidification and the approach to steady-state pH levels. For most buffer species, tracer efflux out of the lumen was compared with changes in buffer concentration as derived from calculations based on the Henderson Hasselbalch equation. Steady-state luminal pH was similar for most buffer systems studied. However, secretory hydrogen ion fluxes into the lumen were significantly higher for permeant than for less permeant buffers. The most likely explanation is that permeant buffers behave as "open" systems maintaining constant low diffusible acid levels in the lumen, whereas impermeant buffers behave as "closed" systems in which non-ionized acid levels are maintained at higher levels. A behavior consistent with this thesis was directly demonstrated for glycodiazine and, to a lesser degree, for DMO. In contrast, phosphate and creatinine behave like buffers in a "closed" system. Characteristics of proximal tubular acidification, of buffer reabsorption, and the effect thereupon of carbonic anhydrase inhibitors are satisfactorily explained by an essential role of (1) hydrogen ion secretion, (2) pK differences, and (3) different permeance of the non-ionized buffer species. However, specific transport mechanisms may, in addition, also contribute to differences in transepithelial buffer movement.

Animals↗

Hypothalamic stimulation and electrolyte excretion: a micropuncture study.

The anterior part of the lateral hypothalamus was stimulated by injection of carbachol through a stereotaxically implanted cannula in the rat. Re-collection micropuncture experiments showed that this procedure, which leads to diuresis and natriuresis with only transient changes in glomerular filtration rate and renal plasma flow, reduced the TF/P inulin ratio along proximal and distal tubules without significant alteration of single nephron glomerular filtration rate in most experimental groups. Fractional proximal sodium reabsorption was significantly reduced from 0.54 +/- 0.02 to 0.34 +/- 0.05. Treatment with DOCA, vasopressin, and oxytocin caused natriuresis, but additional hypothalamic stimulation (HS) led to further reduction in TF/P inulin ratio and proximal fractional sodium reabsorption from 0.42 +/- 0.03 to 0.33 +/- 0.03. Fluid transport across proximal and distal epithelium was also studied by the split-droplet method. It was markedly reduced in both segments after HS. During hormone treatment only distal segments showed reduction of fluid transport by HS. These experiments indicate that HS caused inhibition of fluid transport in the proximal and distal tubule. This effect was only partly due to the liberation of neurohypophysial hormones, since during their administration an additional effect of HS was still observed.

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Sodium in renal tubular acidification kinetics.

Renal proximal tubules and their peritubular capillaries were perfused with mammalian Ringer solutions containing different sodium concentrations. In stop-flow microperfusion experiments, the pH was measured by means of antimony microelectrodes, permitting calculation of rates of H ion secretion and bicarbonate reabsorption. These rates, as well as transepithelial pH and bicarbonate gradients, were significantly reduced at ambient concentrations of 20 and 4 meq/liter Na+. However, even at the lowest sodium concentrations (4 meq/liter), H ion secretion was still 74%, and bicarbonate reabsorption of 64% of control rates. In similar conditions, sodium reabsorption as measured by the split-droplet technique fell to practically zero. Ouabain, 10(-3) M, in capillaries reduced bicarbonate reabsorption by 31%, and 3 X 10(-4) M furosemide in lumen and capillaries reduced acidification by 29%. At pH 8--9 in capillaries, sodium transport was normal while acidification was markedly reduced. These data show that low sodium levels impair renal tubular acidification, but they do not support a rigid coupling of these transport processes.

Animals↗