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O M Sejersted

Publications and source records attributed to O M Sejersted.

119 records · Page 7Linked to original sources
PubMed1978

Functional differences of ouabain and ethacrynic acid on renal potassium metabolism in dogs.

Current concepts provide inadequate explanations for the effects of ethacrynic acid (ECA) and ouabain (OUA) on renal potassium metabolism because neither the site of action, nor the tubular effects have been agrreed upon. In the present study on anaesthetized dogs, in vivo inhibitory effects of ECA on mitochondria or Na-K-ATPase were excluded. Firstly, ECA hardly reduced outer medullary metabolic rates in kidneys exposed to OUA and 2,4-dinitrophenol. Secondly, whereas OUA reduced renal Na-KATPase activity by 78% and induced parenchymal potassium release into the renal vein, none of these effects were observed during injection of ECA. During free flow, sodium reabsorption was equally reduced by the two drugs, but fractional potassium excretion was 0.54 +/-0.04 after OUA and 0.99 +/-0.02 after ECA. OUA alone or combined with ECA inhibited almost all ion transport in the distal 60% of the tubular volume as revealed by stop-flow. During ECA alone, chloride reabsorption was reduced more than sodium reabsorption because sodium was exchanged for potassium. ECA and SO4(2-) infusion produced similar stop-flow patterns. Thus, OUA is bound to Na-K-ATPases functionally located to the peritubular cell membrane. ECA promotes potassium secretion probably by inhibiting cellular anion entry at the luminal membrane.

Adenosine Triphosphatases↗
PubMed1977

Renal Na-K-ATPase activity during saline infusion in the rabbit.

During saline infusion, sodium reabsorption (RNa) in the diluting segment (thick ascending limb of Henle's loop) increases acutely. The mechanism for this higher pumping rate of outer medullary Na-K-ATPase is unknown. Following left-sided nephrectomy, immediate i.v. infusion of hypertonic saline increased RNa in the remaining whole right kidney by 28 +/- 14% (p less than 0.05). Na-K-ATPase activity in outer medulla was raised by (delta) 23 +/- 4% above the left kidney (p less than 0.05), whereas cortical activity was unchanged. The mechanism for this increase in Na-K-ATPase activity was explored. The catalytic rate per enzyme did not differ in the two kidneys and equalled 5 340 min-1. The increase was therefore due to higher tissue concentration of active enzyme. The response was fully developed during continuous infusion within 20 min, and of equal magnitude whether protein synthesis had been inhibited by cycloheximide (delta = 23 +/- 7%) or stimulated by unilateral nephrectomy 6 days earlier combined with saline infusion for 2 h (delta = 34 +/- 10%). Thus, during hypertonic saline infusion, the increased RNa in the outer medulla was partly accounted for by the activation of latent Na-K-ATPase. High delivery of sodium to the diluting segment for more than 20 min during hypertrophy caused no further activity change.

Adenosine Triphosphatases↗
PubMed1977

Oxygen requirement of renal Na-K-ATPase-dependent sodium reabsorption.

The oxygen requirement of the Na-K-ATPase-dependent sodium transport system was examined in anesthetized dogs infused with 15% mannitol-Ringer solutions at a rate of 35 ml/min. Because of renal vasodilatation and abolished autoregulation, filtered sodium (FNa) could be varied over a wide range by progressive aortic constriction. Sodium reabsorption (RNa) and renal oxygen consumption (RVO2) varied in proportion to FNa (r greater than 0.9). Ouabain, which inhibits Na-K-ATPases, reduced RVO2 by 45 +/- 6%. During subsequent aortic constriction, the ratio delta RNa/delta FNa averaged 0.45 (glomerulotubular balance) (r less than 0.9), whereas RVO2 was not significantly altered. Comparisons of deltaRNa/deltaFNa before and after ouabain administration, indicate that about half of an increase in sodium delivery to the distal nephron is reabsorbed by the Na-K-ATPase-dependent sodium transport system and that deltaRNa/deltaRVO2 (Na/O2 ratio) of this system averages 14.5 +/- 1.3. This Na/O2 ratio corresponds to 2.4 sodium ions transported per ATP dephosphorylated as found in other tissues.

Adenosine Triphosphatases↗
PubMed1976

Effect of acetazolamide on glomerular balance and renal metabolic rate.

Glomerulotubular balance, defined as proportionality between filtered and reabsorbed sodium during inhibition of sodium reabsorption in the thick ascending limb of Henle's loop (diluting segment), was examined in anaesthetized dogs by gradual reduction of renal arterial pressure. In control experiments, glomerulotubular balance applied over the whole rante of glomerular filtration rate (GFR) examined but was absent after acetazolamide administration (30 mg/kg/body wt) at GFR above 50% of control. Hence, the inhibitory effect of acetazolamide varied with GFR. At control GFR, acetazolamide reduced tubular sodium reabsorption by 32 +/- 2% chloride reabsorption by 34 +/- 3%, and bicarbonate reabsorption by 52 +/- 2%; no significant effect was observed at GFR below 50% of control. For each bicarbonate ion, three sodium ions and two chloride ions were inhibited. Measurements of renal oxygen consumption and heat accumulation rates showed that acetazolamide did not reduce renal metabolic rate significantly. It is proposed that energy-requiring hydrogen ion secretion occurs at unchanges rate during variations in GFR but that back leakage of hydrogen ions varies with bicarbonate concentration in tubular fluid. Net secretion of hydrogen ions is associated with bicarbonate transport into the intercellular space and is linked with sodium reabsorption. The concentration difference of bicarbonate salts over the tight junction (zonula occludens), which is much less permeable to bicarbonate than to sodium chloride, provides the osmotic force for reabsorption of water and sodium chloride from the tubular lumen into the intercellular space. Glomerulotubular balance is mediated by variations in filtered amounts of bicarbonate.

Acetazolamide↗
PubMedDate not supplied

Methanol poisoning.

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Acidosis↗