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Biomedical subjects

J Diezi

Publications and source records attributed to J Diezi.

30 records · Page 2Linked to original sources
PubMed1980

Urinary enzyme excretion and changes in renal functions induced by toxic substances or by renal ischemia in rats.

The urinary excretion of four enzymes (alkaline phosphatase: AP, leucine aminopeptidase: LAP, lactate dehydrogenase: LDH, muramidase: M) was measured in unanesthetized adult male Wistar rats within 48 h after either a single injection of mercuric chloride (HgCl2) (0.5-1.0 mg x kg-1), or of gentamicin (2.5-25 mg x kg-1), or of tobramoycin (2.5-25 mg x kg-1), or after 30 min of clamping of both renal arteries. Glomerular filtration rate (GFR), TmPAH, plasma urea, urinary protein and sodium excretion were measured simultaneously. The excretion of AP, LAP and LDH, but not that of M, increased significantly above control levels after renal ischemia or the nephrotoxic agents; the increase was dose-related after HgCl2. GFR was not depressed, but TmPAH decreased after the higher doses of the toxic agents. Though more sensitive for detecting minor grades of acute renal damage than function tests, measurements of urinary enzyme excretion were fraught with large inter-individual variation, and variable time-course of changes in different types of renal damage. Short-term exposure (3 months) to phenylmercuric acetate was associated with a significant decrease of the urinary excretion of AP, and of LAP, and of AP activity measured histochemically in proximal tubular cells.

Acute Disease↗
PubMed1980

Inhibition of the anti-natriuretic action of aldosterone by thyroid hormone in the rat.

Urinary sodium excretion was measured in adrenalectomized, euthyroid rats, within 4 hours after injection of aldosterone and/or thyroid hormone (T3). Rats which received both hormones excreted significantly more Na than rats injected with aldosterone alone. Reverse-T3 did not affect the antinatriuretic action of aldosterone. Natriuresis following injection of T3 alone was similar to that measured in the absence of exogenous hormones. These observations suggest an interaction between aldosterone and T3 on renal Na excretion.

Aldosterone↗
PubMed1980

Distal tubular function in superficial rat tubules during volume expansion.

Free-flow micropuncture experiments were carried out on superficial late proximal and distal tubules during hydropenic conditions and during extracellular volume expansion. Fluid collected from tubules was analyzed for inulin and sodium. During volume expansion, renal perfusion pressure to one kidney was reduced so that the increase in distal sodium and fluid delivery that normally occurs after saline loading was prevented. Although urinary sodium excretion remained significantly elevated in such kidneys, the rate of sodium reabsorption along the distal tubules was not different from that occurring under nondiuretic conditions. It is concluded that those factors that reduce net sodium transport in the proximal tubule during extracellular volume expansion do not act on superficial distal tubules. Additional factors beyond the distal tubule contribute to increased sodium excretion and can be shown to be activated even when delivery of fluid and sodium out of superficial distal tubules is normal.

Animals↗
PubMed1978

Interactions between volume expansion or diuretics and compensatory adaptation.

Glomerular filtration rate, urine flow, and Na excretion were measured 3--4 h after unilateral nephrectomy (1/2Nex) or sham operation in unanesthetized rats infused with isotonic saline (0.05--0.75 ml/min) and additionally injected with acetazolamind (20 mg/kg i.p.) or furosemide (5 mg/kg i.p., or 0.2 mg/kg i.v., or 2.0 mg/kg i.v.) or with both agents. Glomerular filtration rate of unilaterally nephrectomized rats averaged 50% of controls. Under all experimental conditions investigated, absolute water and Na excretions were similar in 1/2Nex and sham-operated rats. The fractional excretion (FE) of water and Na was increased 1.5- to 2.2-fold in 1/2Nex animals. The diuretic effects of volume expansion, of the two diuretic agents, and of contralateral nephrectomy consistently were additive. The "compensatory" increase of FESa following contralateral nephrectomy entailed a proportional increase of the diuretic effects of agents given subsequently. Urinary furosemide excretion 15 min after intravenous injection in unilaterally nephrectomized rats was smaller than in controls. The additivity of the diuretic effects of contralateral nephrectomy ("compensatory adaptation") and volume expansion and/or diuretic agents appears to be partly explained by different sites of action.

Adaptation, Physiological↗
PubMed1976

Effects of nephrectomy on renal salt and water transport in the remaining kidney.

Fluid, sodium, and potassium transport was studied in proximal and distal tubules in rats in which one kidney had been removed two weeks after a suprarenal aortic clamp had been placed to prevent adaptive changes in glomerular filtration rate (GFR) in the experimental kidney. Free-flow micropuncture techniques were used and tubular fluid (TF) samples analyzed for inulin, sodium and potassium. In addition, peritubular total protein concentrations and luminal and peritubular hydrostatic pressures were measured. The following changes were observed 15 hr after unilateral nephrectomy: (1) a significant increase in single nephron GFR; (2) unchanged absolute proximal tubular reabsorption rates of fluid and sodium; (3) increased delivery of fluid into distal tubules; (4) increased distal tubular reabsorption of sodium, but of insufficient magnitude to prevent natriuresis; and (5) an augmentation of distal tubular potassium secretion. Reduction of single nephron GRF to control levels by aortic clamping abolished the natriuresis following nephrectomy.

Animals↗
PubMed1976

[Pharmacologic modifications of renal tubular transport].

Possible mechanisms of transport of substances across renal tubular walls and of drug actions influencing these transports are discussed. The precise mechanisms of action of the majority of compounds which enhance or depress transtubular transports is still unknown. Certain inhibitors of transtubular transports may be competitors of the transported substances for tubular membrane carriers. Examples of changes in transtubular transports induced by drugs are reviewed. In the rat, the combined natriuretic and diuretic effects of furosemide and of compensatory adaptation, i.e. removal of the contralateral kidneys a few hours before the experiments, appear to be hyperadditive. The natriuretic and diuretic effects of acetazolamide are similarly enhanced under the conditions of compensatory adaptation. The data suggest that the natriuretic and diuretic effects of compensatory adaptation, on the one hand, and the diuretic agents, on the other hand, are due to different primary effects on the tubules. Bidirectional transports of uric acid across the walls of proximal convoluted tubules have been demonstrated in all species of animals investigated by micropuncture, microperfusion and microinjection. No net movements of uric acid occur across the wall of distal convoluted tubules. In species and under conditions of net reabsorption of uric acid by the whole kidney, the sum of the bidirectional transports across the walls of proximal convoluted tubules always results in pronounced net reabsorption. In species and races of animals characterized by overall tubular secretion of uric acid, the predominant movement in proximal convoluted tubules also tends to be net reabsorption, while the net secretion providing the amounts of uric acid, above the amounts filtered, appearing in the final urine, appears to occur in the straight parts of the proximal tubules. Possible mechanisms of action and micropuncture observations on the sites of actions of probenecid and of pyrazinolic acid, two agents which influence transtubular transports of uric acid, are discussed. The conclusion is reached that agents influencing transtubular uric acid transports probably always act on reabsorptive as well as on secretory transports and that the net result of their action on uric acid excretion may, therefore, vary in different species and under different experimental conditions. Enhancement of the urinary excretion of salicyclic acid by infusion of bicarbonate is a well-known fact. Recent micropuncture experiments indicate that this effect is probably due to either enhanced secretion or depressed reabsorption of salicylates in proximal convoluted tubules rather than on any changes of the rate of transtubular salicylate transports in lower segments of the nephron.

Acetazolamide↗
PubMed1975

Some aspects of proximal tubular sodium chloride reabsorption in Necturus kidney.

Some aspects of proximal tubular sodium chloride reabsorption in Necturus kidney. Renal tubular reabsorption of fluid and sodium was measured by clearance methods in the doubly perfused Necturus kidney in which the bicarbonate concentration was varied between 0 and 60 mEq/liter. The effects of Damox (2.2 times 10-3M), ocubain (10-5M) and ethacrynic acid (10-4M) and of acidosis were also investigated. In addition to clearance experiments, stationary microperfusion experiments were carried out on promimal tubules to measure volume flow and steady-state sodium and chloride concentration differences across the tubular epithelium. In some experiments, the transepithelial electrical potential difference was also measured using an axial electrode system. The following results were obtained: 1) Bicarbonate is not essential to the operation of renal tubular fluid and sodium transport. 2) Total renal and proximal tubular fluid and sodium transport are partially inhibited by Diamox, ouabian and ethacrynic acid. 3) The proximal tubule maintains a significant transepithelial sodium and chloride concentration difference and a significant electrical potential difference (lumen-negative) in the presence of a poorly permeant nonelectrolyte. The direction and magnitude of the electrical polarization fully accounts for the observed chloride concentration difference. The data support the thesis that sodium chloride transport accross the proximal tubular epithelium takes place by active sodium transport and electically coupled passive chloride reabsorption. Important species differences with respect to mammalian transport mechanisms are discussed.

Action Potentials↗
PubMedDate not supplied

Studies on possible mechanisms of early functional compensatory adaptation in the remaining kidney.

Two to 4 hours after unilateral renal exclusion in rats, urine flow rate from the remaining kidney had increased to twice the control level, whereas the filtration rate remained unchanged. After contralateral nephrectomy, NGFR was similar to that of controls, but fractional water reabsorption along proximal tubules decreased. Protein concentration in efferent arteriolar plasma, and hydrostatic pressure gradient between proximal tubules and peritubular capillaries were similar in experimental and control kidneys. Unilateral renal exclusion was followed by a rapid increase of blood pressure. Prevention of this rise depressed but did not abolish functional compensatory adaptation. The occurrence of compensatory adaptation was not affected by decreased renal perfusion pressure.

Adaptation, Physiological↗