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Biomedical subjects

E A Alexander

Publications and source records attributed to E A Alexander.

76 records · Page 5Linked to original sources
PubMed1971

Proximal tubular function in dogs with thoracic caval constriction.

The effect of saline infusion on proximal sodium reabsorption was compared in normal dogs and in dogs with acute or chronic partial thoracic vena cava obstruction. After acute vena cava obstruction, proximal fractional sodium reabsorption rose by 74%. During continued caval obstruction, saline loading strikingly reduced proximal reabsorption but sodium excretion remained minimal. In chronic caval dogs, saline loading reduced proximal fractional sodium reabsorption by 31% but sodium excretion in the micropunctured kidney was only 41 muEq/min. After saline infusion in normal dogs, proximal fractional sodium reabsorption fell 39% while unilateral sodium excretion rose to 584 muEq/min. Nephron filtration rate was also measured before and after saline loading in normal and chronic caval dogs in both repunctured and fresh tubules. There was a marked increase in nephron filtration rate in repunctured tubules and no change in freshly punctured tubules in both groups. The effect of saline loading on nephron filtration rate in normal and chronic caval dogs was similar, therefore, whether repunctured or fresh nephrons were considered.We conclude that saline infusion depresses proximal sodium reabsorption in acute and chronic TVC dogs. Since saline loading markedly increases distal delivery without a concomitant natriuresis, enhanced distal reabsorption must play a major role in the sodium retention exhibited by chronic caval dogs. Redistribution of filtrate does not appear to be a factor in this sodium retention.

Aminohippuric Acids↗
PubMed1968

An extrarenal mechanism of potassium adaptation.

Rats fed a diet high in potassium for several days survive an acute load of potassium that is lethal to animals on a regular diet. Previous data suggested that this survival occurred because of enhanced kaluresis. Although increased urinary excretion may occur, the major mechanism of this potassium adaptation phenomenon has been found to be extrarenal. Despite nephrectomy just before study, rats previously fed a high potassium diet maintained lower plasma potassium concentrations for at least 2 hr after an acute potassium load than did rats fed a regular diet. Prior adrenalectomy abolished adaptation. Furthermore, rats fed a low sodium diet as an alternative stimulus to aldosterone secretion demonstrated adaptation to potassium loading, as did adrenalecomized rats given large doses of deoxycorticosterone for several days. Adrenalectomy just before the test load of potassium did not abolish adaptation nor did a large dose of aldosterone at that time reproduce it. These data indicate that adaptation is dependent on a chronic increase in aldosterone secretion. The extra potassium removed from the extracellular fluid by adapted rats was not lost into the gastrointestinal tract. It is concluded that more rapid lowering of plasma potassium after acute potassium loads by adapted rats is due to enhanced uptake of potassium by one or more tissues stimulated by chronic aldosteronism.

Adaptation, Physiological↗