Erythrocyte Urea Research Articles

Urinary concentrating ability in patients with Jk(a-b-) blood type who lack carrier-mediated urea transport.

Water homeostasis is regulated in large part by the proper operation of the urinary concentrating mechanism. In the renal inner medulla, urea recycling from the inner medullary collecting duct to the inner medullary interstitium is thought to be essential for the production of a concentrated urine; however, it has not been possible to test this hypothesis in humans. Recently, a unique combination of genetic abnormalities has been described: absence of Kidd blood group antigens and absence of carrier-mediated urea transport in erythrocytes. Because animal studies indicate a similarity between urea transport in red blood cells and the nephron, it was postulated that patients without the Kidd antigen might lack facilitated urea transport in their kidneys. Hence, their ability to concentrate urine maximally was measured. Current models of nephron function would predict that in the complete absence of urea transport, the maximal concentrating ability would be around 800 to 900 mosM/kg H2O. Two homozygous patients had a moderate decrease in maximal concentrating ability (UosM,max = 819 mosM/kg H2O); a heterozygote also had some limitation. These studies raise the possibility that the erythrocyte urea transporter and the kidney urea transporter are encoded by a single gene (detected by the mutational loss of the Kidd antigen) and that a lack of facilitated urea transport impairs urea recycling in the kidney and, hence, maximal urinary concentrating ability.

A method to distinguish between pore and carrier kinetics applied to urea transport across the erythrocyte membrane

Permeability coefficients ( P) measured at various penetrant concentrations ( C) by the perturbation method can be plotted to distinguish simple diffusion, simple pore kinetics and simple carrier kinetics as follows: for simple diffusion, 1/ P = constant; for a simple pore, 1/ P = 1/ P 0 + 1/ P 0[1/ K in + 1/ K 0] C; for a simple carrier, 1/ P = 1/ P 0 + 1/ P 0[1/ K in + 1/ K 0] C + 1/ P 0[1/( K 3 K 4)] C 2 where P 0 is the maximal permeability at zero penetrant concentration and the K's are combinations of kinetic constabts defining each of the transport steps. ( K inand K 0 are the half-saturation constant for zero-trans efflux and influx, respectively; K 3 is the half-saturation constant for equilibrium exchange, and K 4 is related to the mobility of the free carrier.) In human erythrocytes, permeability coefficients for diethylene glycol were constant suggesting simple diffusion. For glucose, a plot of 1/ P versus concentration was nonlinear indicating carrier kinetics. Plots of 1/ P versus penetrant concentrations gave straight lines with positive slopes for urea in human and bovine erythrocytes and for methylurea in human red cells, indicating these penetrants follow simple pore kinetics or simple carrier kinetics in which K 4 is very large.

Effect of Vasopressin on the Permeability of Non Electrolytes Across the Skins ofRana EsculentaandBufo Bufo

Maximal doses of vasopressin increase the permeability of the skins of Bufo bufo and Rana esculenta to urea, ethylene glycol, glycerol, erythritol, beta-alanine, leaving virtually unmodified that of mannitol and antipyrine. These results demonstrate that the response to vasopressin is quite different in amphibian skins as compared to the bladders. A careful analysis of the effects of vasopressin on non-electrolyte permeability as a function of their molecular weight demonstrates that hormone elicits the formation of pores with a diameter inferior to 4 A. Under vasopressin treatment the skins exhibit a selectivity for polyhydroxylated molecules as compared to urea and beta-alanine. This selectivity is not due to active of facilitated transport and is not impaired by phloretin or DTNB which selectively blocks the permeability of urea or ethylene glycol in erythrocytes. It is proposed that the site of such selectivity is located in other plasma membranes of the epithelium.

Urea movement across erythrocyte membrane during artificial kidney treatment

Previous work by other investigators indicates that erythrocyte urea and creatinine in uremic whole blood leaving the hemodialyzer do not move down the concentration gradients established by loss of these solutes across the dialyzer membrane. This puzzling disequilibrium is at odds with work indicating ready movement of both solutes across the erythrocyte membrane of nonuremic erythrocytes studied in vitro. The present study shows that contact with the dialyzer does not noticeably alter the erythrocyte membrane of the uremic patient, so that urea distribution between plasma and erythrocyte water is the same as that in the blood of normal control subjects. Furthermore, urea does not show a disequilibrium in concentration across the erythrocyte membrane in response to 50% dilution with a modified Ringer's solution but rather equilibrates swiftly and completely.

Urea levels in plasma and erythrocytes of the southern fiddler skate, Trygonorhina fasciata guanerius.

Plasma and erythrocyte samples from Trygonorhina fasciata guanerius were analysed for urea content. The erythrocyte urea concentration is higher than plasma urea concentration. The difference in concentration is probably due to the presence of urea normally bound to protein within the erythrocyte. Erythrocyte urea concentrations followed environmentally induced changes in plasma urea concentrations. Naturally occurring plasma urea concentrations, exceeding 500 mMolar, are some of the highest recorded for an elasmobranch.

Hemolysis of elasmobranch erythrocytes in urea solutions: effect of temperature.

AbstractSkate and stingray cells were shown to hemolyze in isosmotic solutions containing urea as the sole solute. The rate of urea penetration into these cells as determined by the rate of hemolysis is highly temperature dependent with a Q10 of 2.50–2.75. A reduced rate of methylurea penetration in the presence of urea was reconfirmed. The present results are consonant with the hypothesis of carrier mediated transport of urea in elasmobranch erythrocytes previously proposed by Murdaugh, Robin and Hearn.

The formation of urea in human erythrocytes

The formation of urea was studied in mature erythrocytes under different conditions. The hemolyzed erythrocytes can produce urea in the presence of magnesium ions and adenosinetriphosphate, citrulline and aspartic acid. The highest formation of urea found was 943 μmoles/100 ml of packed erythrocytes/16-h incubation. Admixtures of leucocytes and reticulocytes were found not to be responsible for this formation of urea.

Erythrocyte volume and urea in elasmobranchs.

Erythrocyte volume and urea in elasmobranchs.