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B Corman

Publications and source records attributed to B Corman.

80 records · Page 5Linked to original sources
PubMed1981

Water reabsorption capacity of the proximal convoluted tubule: a microperfusion study on rat kidney.

1. The differences in the water reabsorption capacity observed from one proximal tubule to another were investigated in vivo by continuous microperfusion. 2. Two to seven loops were punctured along the same tubule. The [3H]inulin, 22Na, [14C]glucose, sodium, chloride and magnesium concentrations as well as the osmolality of the collected samples were studied as a function of the perfused length. 3. With Ringer bicarbonate solution perfused in Saclay Wistar rats, the water reabsorption capacity ranged from 0 to 3 nl . min-1 . mm-1 depending on the tubule. This reabsorption rate was closely correlated with the unidirectional reabsorption flux of sodium, and with the rise in tubular chloride and magnesium concentrations. 4. In Munich Wistar rats with glomeruli accessible at the kidney surface, tubule perfusion with a Ringer bicarbonate solution showed that the highest water reabsorption rates per mm of tubule were found for the perfusion sites closest to the glomerulus; water fluxes were also positively correlated with glucose transport. 5. In a second series of experiments on Saclay rats, perfusion of a Ringer solution containing a high chloride concentration (137 m-equiv/l.) was unable to increase the water reabsorption rate compared to the control perfusion; here again, water fluxes were positively correlated with glucose transport.

Absorption↗
PubMed1980

Proximal tubular response to variations in extracellular sodium concentration.

In vitro microperfusion was used to study the effect of low and high extracellular sodium concentrations on the transport capacity of the proximal convoluted tubule (PCT). Tubules from rabbit kidney were perfused with luminal and peritubular solutions containing 80, 115, 190, and 225 mM sodium. Control solutions contained 150 mM sodium. No ionic substitution was made and the proximal convoluted tubules were studied under hypo- or hypertonic conditions after a 20-min equilibration period. Sodium concentration was measured at 80, 150, and 225 mM sodium in the perfused and collected fluids and no significant difference was observed. Net sodium transport (JNa) remained relatively constant between 115 and 150 mM sodium. It decreased progressively at high sodium concentrations. Depression in JNa was also observed at 80 mM sodium. Fractional sodium reabsorption increased to 125.0% of control at 115 mM sodium and decreased to 69.4 and 40.1% at 190 and 225 mM sodium, respectively. At 80 mM, the results were not different from control. These findings indicate that at concentrations of 115-225 mM sodium the proximal convoluted tubule has the intrinsic capacity to regulate sodium transport.

Animals↗
PubMed1978

Glucose-mediated inhibition of phosphate reabsorption in rat kidney.

Clearance, tracer intra-arterial injection, and tracer intratubular microinjection techniques were used on two strains of Wistar rats. In Saclay rats, clearance studies during hyperphosphatemia showed that glucose significantly decreased reabsorption of phosphate; during normal phosphatemia, glucose induced a 25% inhibition both in nondiuretic and in volume-expanded animals; thyroparathyroidectomy did not modify this inhibition. When mannitol was substituted for glucose, no change in phosphate reabsorption was noted. Tracer injection into the renal arteries of [3H]inulin, [14C]glucose, and [32P]-phosphate with or without additional unlabeled glucose or mannitol showed that the presence of glucose significantly increased 14C and 32P urinary recoveries but not mannitol. Intratubular paired microinjections into early proximal tubules of the same tracers with and without glucose showed that addition of sugar also increased the 14C and 32P urinary recoveries. In Munich rats, the effects were much less marked than in Saclay rats. It is concluded that the inhibitory effect of glucose 1) partly results from intrarenal factors, 2) is linked to glucose reabsorption per se but not to a nonspecific osmotic intraluminal effect, 3) is localized on the tubular luminal side, and 4) is subject to strain differences.

Animals↗
PubMedDate not supplied

Quantitative analysis of the Purkinje cell population during extreme ageing in the cerebellum of the Wistar/Louvain rat.

The loss of neurons is viewed as one of several causes of the deterioration of neural function during ageing. However, the existing experimental evidence for an age-related decrease in the neuronal number may be misinterpreted due to the way the cells are counted and to the interference of unsuspected degenerative pathology of the animals studied. To reinvestigate this question we have quantified an easily identifiable population of neurons, the cerebellar Purkinje cells, in very old but healthy rats. The number of Purkinje cells in the cerebellum was assessed in two populations of rats: control (10 months) and old (42 months) rats from the Wistar/Louvain strain. In both groups, paraffin-embedded brains were cut serially in the sagittal plane. Purkinje cells were counted every 15 or 22 sections under the light microscope at a magnification of 1250 x. The raw value of cell counts were corrected according to the method of Hendry (21) in order to avoid the overestimation due to splitting of the nucleus during sectioning. The latero-lateral extent of the cerebellar cortex, obtained by multiplying the thickness of the section by the number of sections in which Purkinje cells were counted, was not statistically different (mean +/- standard deviation): 12.8 +/- 1.16 mm (n = 6) for the control rats and 12.0 +/- 1.02 mm for the old animals (n = 8) (Student's t-test, p = 0.18). The corrected number of the Purkinje cells (mean +/- standard deviation) was 330,350 +/- 35,448 cells (n = 6) for the control animals and 299,019 +/- 50,223 (n = 8) cells for the old rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMedDate not supplied

Endothelium-dependent changes in arterial diameter in old normotensive rats.

1. In normotensive rats, removal of carotid artery endothelium results in an acute increase in diameter. This finding, observed in young animals, has not been investigated in old animals. The present study was undertaken to assess the contribution of endothelial function in the regulation of arterial stiffness in aged rats. 2. In normotensive female WAG/Rij rats, isobaric (100 mmHg transmural pressure) carotid diameter was measured in vitro in situ, using a previously described arterial preparation associated with a high-resolution echotracking technique allowing non-invasive diameter measurements under baseline conditions, after removal of the endothelium and after total relaxation of vascular smooth muscle by potassium cyanide. Histomorphometry of the carotid wall was studied after pressure fixation (100 mmHg) of the arteries. 3. Compared with younger animals (10 months), older animals (30 months) had the same baseline carotid isobaric diameter but significantly higher values of wall thickness and collagen content. In older animals, whereas total relaxation by potassium cyanide was associated with a slight but significant increase of isobaric diameter, no increase was observed after endothelium removal. 4. The results of the presnt study provide evidence that, in old normotensive rats, endothelium-dependent increases in isobaric carotid diameter are blunted. This endothelium alteration may contribute to the age-dependent increase in isobaric carotid stiffness observed in old rats.

Aging↗
PubMedDate not supplied

[Kidney aging: cellular mechanisms of problems of hydration equilibrium].

The ability to control body hydration is frequently impaired with age. This mainly results from changes in thirst and from loss of renal concentrating ability. The cellular mechanisms responsible for this functional renal failure have been extensively studied in different experimental models. Although the loss of nephrons sometimes observed with age impairs the ability of the kidney to retain water, a similar defect was reported in animals free of glomerulosclerosis, indicating that the reduction in the number of nephrons was not the only cause. Because age-related polyuria has also been demonstrated in rats with unchanged secretion of vasopressin, renal changes in water reabsorption was hypothesized. Such alterations have been searched along the whole length of the nephron. Neither the single nephron filtration rate nor proximal or early distal flow rates were modified in senescent animals where water reabsorption in the collecting duct was reduced. The affinity and the density of the V2 receptors were mainly constant in most experimental models of ageing. In contrast, intracellular cAMP accumulation following vasopressin stimulation was reduced in the oldest animals. The expression of aquaporins in luminal and basolateral membranes of the collecting duct epithelial cells was altered. The amount of basolateral aquaporin 3 and 4 was respectively decreased by 50 per cent and unchanged in renal papilla. In addition, the expression of aquaporin 2, which is rate limiting for the osmotic permeability of the collecting duct, was reduced by 50 per cent in the outer medulla and by 80 per cent in the inner medulla of the senescent animals. This drop in aquaporin 2 expression in the distal part of the nephron could be the main cause for the fall in concentrating ability of the kidney and the age-related impaired control of hydration.

Aging↗