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Biomedical subjects

A Nizet

Publications and source records attributed to A Nizet.

At least 19 recordsLinked to original sources
PubMed1982

Renal control of the peripheral uptake of exogenous gastrin in the dog.

The extraction of plasma gastrin during intravenous infusion of exogenous hormone has been measured in the head, gastrointestinal tract, or kidney of dogs submitted to sham surgery, evisceration, or binephrectomy without or with subsequent kidney transplantation. A significant gastrin extraction was demonstrated not only in the kidney, but also in the head and in the gastrointestinal tract; moreover, plasma gastrin extraction in the head and the bowel was considerably reduced by binephrectomy and was brought back to control values after subsequent kidney transplantation. A non-specific effect of surgery and a variation in peripheral blood flow seem to be excluded. Thus a control by the kidney of the peripheral removal of blood gastrin is evidenced, the mechanism of which remains hypothetical.

Animals↗
PubMed1981

Influence of uranyl nitrate upon tubular reabsorption and glomerular filtration in blood perfused isolated dog kidneys.

The early changes in tubular reabsorption, glomerular filtration, blood flow and sodium excretion brought about by uranyl nitrate were investigated in isolated, blood-perfused dog kidneys during water diuresis. No significant changes in urine volume were observed; the decrease in fluid reabsorption was counterbalanced quantitatively by a reduction in glomerular filtration rate; only a small diminution of renal blood flow was found. The balance between reabsorption and filtration was observed as well when angiotensin action or prostaglandin synthesis were inhibited. The intrarenal venous pressure rose, suggesting that an increase in proximal intratubular hydrostatic pressure caused the decrease in filtration. Tubular back-leak of fluid, or back-diffusion, induced by the toxin, were excluded. The presence of natriuretic compounds in the urine was confirmed.

Absorption↗
PubMed1981

Connection between the changes in tubular reabsorption and in glomerular filtration rate induced by replacement of plasma sodium and chloride by isotonic mannitol.

Glomerular filtration and tubular reabsorption have been investigated comparatively in isolated blood-perfused dog kidneys, after addition to the blood of equal volumes of isotonic sodium chloride or isotonic mannitol. In the absence of antidiuretic hormone activity, the urine output showed no significant difference, while the glomerular filtration rate was lower in the presence of the mannitol load. The inhibition of fluid reabsorption was compensated by the decrease of filtration; a quantitative tubulo-glomerular equilibrium was evidenced. The fractional sodium excretion was decreased following the dilution by the mannitol load of plasma sodium and -chloride; this difference disappeared when the reabsorption in the diluting segment was inhibited by furosemide, suggesting that it depended on the rate of chloride reabsorption in this part of the tubule.

Animals↗
PubMed1980

The intrarenal regulation of sodium excretion in the dog.

1. The effect of sodium chloride-containing solution (saline) infusion on sodium excretion has been investigated in kidneys transplanted from donors into the neck vessels of other dogs (perfusors). The dogs (perfusors and donors) had been given sodium-enriched or sodium-poor diets ("loaded" and "deprived' dogs). 2. Three series of experiments were performed: (A) loaded perfusor, loaded donor; (B) deprived perfusor deprived donor; (C) deprived perfusor, loaded donor. 3. Kidneys from deprived dogs, transplanted into deprived perfusors, excreted less sodium after intravenous saline than kidneys from loaded dogs transplanted into loaded perfusors. However, the sodium excretion from the kidneys of loaded dogs transplanted into deprived perfusors was the same as that from the kidneys of loaded dogs transplanted into loaded perfusors. These differences suggest that intrarenal mechanisms are involved in the changes in sodium excretion which follow changes in dietary sodium balance. 4. The intraenal mechanisms included changes in glomerular filtration rate and fractional sodium reabsorption, but not changes in filtration fraction or renin release.

Animals↗
PubMed1980

Furosemide, indomethacin and sodium excretion in isolated, blood-perfused dog kidneys.

Sodium excretion, renal blood flow and glomerular filtration rate were investigated in isolated, blood-perfused dog kidneys, thus excluding the interference of changes in body sodium and water balance. Four groups of experiments were performed : (a) control; (b) blood + indomethacin; (c) blood + furosemide; (d) blood + furosemide and indomethacin. The progressive vasodilatation due to the accumulation of prostaglandins was suppressed by indomethacin, the glomerular filtration rate remaining unchanged. The inhibition of prostaglandins synthesis was without influence on the natriuretic activity of furosemide. These results seem incompatible with an intrarenal mediation by prostaglandins of the diuretic effect of furosemide; moreover, this effect was dissociated from the changes in renal blood flow ascribed to renal prostaglandins.

Animals↗
PubMed1979

Inhibition by indomethacin of the renal response to an acute saline load in the dog.

The kidneys of sodium-loaded dogs, treated by indomethacin before their transplantation to the neck vessels of sodium-depleted animals, lose their ability to increase the fractional excretion of sodium following an intravenous infusion of saline; they behave similarly to the kidneys of sodium-depleted dogs. Moreover, they become unable to potentiate the response of the kidneys of the sodium-depleted perfusors. The experimental conditions exclude a direct effect of the drug eo ipso. The results indicate that renal prostaglandins are involved in the adjustment of the renal response to saline loading, depending on the previous dietary sodium balance, and that they are related with the potentiating factors released into the blood by the kidneys of sodium-loaded animals.

Animals↗
PubMed1979

Influence of replacement of chloride by sulphate upon urine excretion and glomerular filtration rate in blood perfused isolated dog kidneys.

Tubular reabsorption was inhibited in isolated dog kidneys by the progressive substitution of plasma chloride by sulphate. In the absence of antidiuretic hormone activity, urine output remained unchanged owing to an equivalent decrease in glomerular filtration rate. This equilibrium was demonstrated under conditions of "saline natriuresis" and was not disturbed by furosemide. Although the impairment of glomerular filtration rate was accompanied by a decrease of total renal blood flow, the equilibrium was not disrupted by angiotensin antagonism. Sodium excretion was enhanced by low plasma chloride concentrations in the absence, but not in the presence of furosemide. The results are not compatible with a specific role of osmolality, sodium or chloride concentrations in the tubular fluid in the adjustment of glomerular filtration. Simultaneous changes in blood flow and tubular flow resistances might explain the results. It is suggested that, in contrast to the mechanism of tubulo-glomerular feedback found in individual nephrons of hydropenic animals, this intrarenal mechanism might serve to protect the organism against sodium loss under conditions of high intake.

Animals↗
PubMed1978

Humoral control by the kidney of intestinal transport to sodium.

The impairment of water and sodium absorption by the jejunum following an acute saline load depends on the dietary balance of sodium, the mucosa-to-serosa unidirectional flux of this ion being modulated by a direct effect of the changes in blood concentration and by a humoral material of renal origin which itself is released as a consequence of either chronic or acute sodium loading. A possible interference of mineralocorticosteroids, angiotensin or antidiuretic hormone seems to be excluded. A positive correlation exists between mucosa-to-serosa sodium flux and glucose absorption. The kidney controls the exchanges of sodium and water in the jejunum as well as in the kidney itself by the way of an endocrine function.

Animals↗
PubMed1976

Renal control of intestinal sodium and water transport in the dog.

The influence of an intravenous infusion of saline on the absorption of water and sodium by the jejunum has been investigated in dogs previously submitted to sodium-rich or poor diets. While the net intestinal transport was reduced in sodium-loaded animals, no response was observed in the sodium-deprived dogs, despite identical changes in arterial pressure, intravascular volume and blood dilution indexes. The intestinal response of sodium-deprived dogs became positive after transplanting to their neck vessels the kidneys removed from sodium-loaded animals, thus demonstrating that the presence in the blood of a humoral message of renal origin is required to permit the inhibition of net transport. The difference of the responses depended on the variations of the mucosa-to-serosa unidirectional flux. The net potassium transport did not change significantly. The experimental conditions made unlikely an interference of mineralocorticosteroids, angiotensin or antidiuretic hormone. The present results suggest that the kidney might modulate sodium transport in the jejunum, and perhaps elsewhere in the body, by the way of an additional endocrine function.

Animals↗
PubMed1976

Comparative evaluation of fractional excretion of sodium following saline infusion in transplanted kidneys and in isolated perfused kidneys in conditions of previous high or low dietary sodium intake.

The increase of fractional excretion of sodium following the infusion of isotonic saline solution is quantitatively the same in dog kidneys perfused by a whole animal or by a pump-oxygenator machine at identical arterial and venous pressures. The equal response found in both experimental conditions demonstrates that the dilution of the blood, and primarily the decrease of post-glomerular plasma oncotic pressure, represents the only extrarenal humoral factor of significant importance in the reduction of fractional reabsorption of sodium following large saline infusion. The renal response to hemodilution is reduced similarly in both types of experiments when the dogs have been previously submitted to a dietary deprivation of sodium. The decreased sensitivity of the kidney to the stimulus of hemodilution appears as a major determinant of the poor natriuretic response to saline loading of sodium-deprived animals.

Animals↗
PubMed1976

Excretion of sodium and water by kidneys in situ and by transplanted kidneys following isotonic, hypotonic, iso-oncotic and hyperoncotic intravenous infusions in sodium-loaded and sodium-deprived dogs.

The excretion of sodium and water following isotonic, hypotonic, iso-oncotic and hyperoncotic intravenous infusions has been investigated in the kidneys in situ and in transplanted kidneys of narcotized dogs previously submitted to sodium-enriched or-deprived diets. The fractional excretion of sodium depended basically on the cumulative effect on the kidney of the changes in plasma oncotic pressure, plasma sodium concentration, and haematocrit. The differences in excretory responses of sodium-loaded or-deprived animals did not depend on differences in the distribution of infused fluids between intra- and extravascular compartments, but to the sensitivity of the kidney itself to the direct cumulative effect of these non-specific changes in blood composition.

Animals↗
PubMed1976

Hormones and non-specific humoral factors in the interferences between sodium, glucose and phosphate handling by dog kidney.

Some relationships between renal handling of sodium, glucose and phosphate have been investigated comparatively in dog kidneys studied "in situ", transplanted to the neck vessels of a perfusor animal, or perfused by a pump-oxygenator machine. The results can be summarized as follows: a) The values of tm of glucose per ml of glomerular filtration rate are not significantly different in the presence or in the absence of a perfusor animal, thus ruling out an hormonal modulation. b) An identical curvilinear regression relation between tmG and fractional excretion of sodium is found in the three types of experiments; the response to saline loading is identical; therefore an hormonal control of extrarenal origin is excluded. The differences in the decrease of tm glucose at high or low values of sodium excretion seem best explained by a coupling between glucose transport and one component of sodium transport which should be comparatively less influenced when the impairment of proximal reabsorption is high. c) A competition between glucose and phosphate excretion is observed in the isolated kidney; therefore it depends also at least for some part on intrarenal mechanisms. d) Insulin decreases phosphate clearance by direct renal action, probably by enhancing the tubular reabsorption of this ion as well as of sodium.

Animals↗