The mechanism of action of mercurial preparations on transport processes and the role of thiol groups in the cell membrane of renal tubular cells

Kleinzeller, A.; Cort, J. H.

doi:10.1042/bj0670015

Cited by 53 publications

(17 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This consideration would hold if C1 were passively distributed across the cell membrane. Bath to cell Cl concentration ratios between 1.5 and 4 have been reported (21,31,32,11) and we have obtained in preliminary experiments ratios between 1.3 and 2 at an external K concentration of 5.3 mmole/kg. These ratios are significantly lower than those expected from a passive distribution of Cl.…”

Section: The Possibility That Some K Is Bound Within the Cellsmentioning

confidence: 86%

Sodium Extrusion and Potassium Uptake in Guinea Pig Kidney Cortex Slices

Whittembury

1965

The Journal of General Physiology

View full text Add to dashboard Cite

Slices from the cortex corticis of the guinea pig kidney were immersed in a chilled solution without K and then reimmersed in warmer solutions. The Na and K concentrations and the membrane potential V,,, were then studied as a function of the Na and K concentrations of the reimmersion fluid. It was found that Na is extruded from the cells against a large electrochemical potential gradient. Q0 for net Na outflux was -2.5. At bath K concentrations larger than 8 mM the behavior of K was largely passive. At the outset of reimmersion (Vm > Ej) K influx seemed secondary to Na extrusion. Na extrusion would promote K entrance, being limited and requiring the presence of K in the bathing fluid. At bath K concentrations below 8 m, K influx was up an electrochemical potential gradient. Thus a parallel active K uptake is apparent. Qo0 for net K influx was -2.0. Dinitrophenol inhibited net Na outflux and net K influx, Q o became <1.1 for both fluxes. The ratio between these fluxes varied. Thus at the outset of reimmersion the net Na outflux to net K influx ratio was > 1. After 8 minutes it was < 1.

show abstract

Section: The Possibility That Some K Is Bound Within the Cellsmentioning

confidence: 86%

Sodium Extrusion and Potassium Uptake in Guinea Pig Kidney Cortex Slices

Whittembury

1965

The Journal of General Physiology

View full text Add to dashboard Cite

show abstract

“…It is also deposited in the liver, muscles, and bones (Dathan, 1954;Polson and Tattersall, 1959b). Mercury has a specific affinity for sulphydryl groups, including those concerned with transport mechanisms across the renal tubular basement membrane (Kleinzeller and Cort, 1957). Burston, Darmady, and Stranack (1958) showed that damage to the convoluted tubules, both proximal and distal, was the salient feature of the acute nephrotoxicity of mercury.…”

Section: Discussionmentioning

confidence: 99%

Infantile Renal Tubular Acidosis Due to Mercury Poisoning

Husband¹,

McKellar²

1970

Archives of Disease in Childhood

View full text Add to dashboard Cite

“…Since mercury poisoning probably inhibits active sodium transport (23), some other driving force must have been responsible for passive movement of water across the epithelium. The only other force of sufficient magnitude to accomplish this is the colloidal oncotic pressure of the peritubular capillary blood, which is equivalent to approximately 35 cm of water (2).…”

Section: Discussionmentioning

confidence: 99%

The Role of “Leakage” of Tubular Fluid in Anuria Due to Mercury Poisoning*

Bank¹,

Mutz²,

Aynedjian³

1967

J. Clin. Invest.

160

View full text Add to dashboard Cite

Summary. The role of "leakage" of tubular fluid in anuria produced by mercury poisoning was studied in rats by micropuncture techniques. After an initial brisk diuresis, almost all animals were completely anuric 24 hours after HgCl2 injection. Lissamine green injected intravenously in the early stage of anuria appeared in the beginning of the proximal tubule, but the color became progressively lighter as the dye traversed the proximal convolutions. The dye was barely visible in the terminal segments of the proximal tubule; it did not appear at all in the distal tubules. These observations suggest that the proximal epithelium had become abnormally permeable to Lissamine green.Tubular fluid to plasma inulin (TF/PIn) ratios and inulin clearance were measured in individual nephrons at three sites: early proximal tubule, late proximal tubule, and distal tubule. It was found that TF/PN ratios were abnormally low in the late proximal and distal tubules. Inulin clearance was normal at the beginning of the proximal tubule but fell by more than 60% by the late proximal convolutions. Thus, the proximal tubule had also become permeable to inulin.We conclude from these observations that anuria in mercury poisoning can occur in the presence of a normal glomerular filtration rate. The absence of urine flow appears to be due to complete absorption of the filtrate through an excessively permeable tubular epithelium. The driving force affecting this fluid absorption is probably the colloid oncotic pressure of the peritubular capillary blood. IntroductionThe pathologic physiology of anuria in acute renal failure remains obscure in spite of extensive study. The three mechanisms that have been postulated are: a severe reduction in renal blood flow and glomerular filtration rate (GFR), obstruction of the tubules by casts or edema, and excessive

show abstract

The mechanism of action of mercurial preparations on transport processes and the role of thiol groups in the cell membrane of renal tubular cells

Cited by 53 publications

References 21 publications

Sodium Extrusion and Potassium Uptake in Guinea Pig Kidney Cortex Slices

Sodium Extrusion and Potassium Uptake in Guinea Pig Kidney Cortex Slices

Infantile Renal Tubular Acidosis Due to Mercury Poisoning

The Role of “Leakage” of Tubular Fluid in Anuria Due to Mercury Poisoning*

Contact Info

Product

Resources

About