English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

This study was prompted by three problems: 1) the role of vasopressin in the countercurrent mechanism for concentrating urine; 2) the effect of dehydration on this mechanism; and 3) the behavior of this mechanism in the absence of vasopressin when the body fluid volumes are contracted rather than expanded. Although it is generally accepted that counter-current systems in the renal medulla effect the concentration of urine, several questions about the operation of these systems remain unanswered (1). For example, it is not known whether vaso-pression enhances the sequestration of nonurea solutes in the medullary interstitium, either by increasing the reabsorption of sodium from the loops of Henle, by slowing medullary blood flow, or both. Levitin, Goodman, Pigeon, and Epstein demonstrated a progressive and significant increase in sequestered sodium within the renal papilla and medulla of dogs as vasopressin was superimposed on a water diuresis by intravenous infusion (2). Since they also found the enrichment of papillary and medullary sodium by infused 22Na to be more rapid during water diuresis than during antidiuresis, they suggested that vasopres-sin may promote medullary sequestration of sodium by slowing medullary blood flow, not by increasing reabsorption of sodium from the ascending loops of Henle. In contrast, Jaenike has presented indirect evidence suggesting that vasopres-sin does not enhance the medullary sequestration of nonurea solute (3). Although other investigators have reported similar studies (4, 5), there still is no agreement whether or not vasopressin promotes the medul-lary sequestration of sodium. The availability of rats with a genetic, apparently absolute, defect for synthesizing vasopressin (6) seemed to present an ideal opportunity for reinvestigating this problem. If vasopressin promotes the medullary sequestration of sodium, one might predict that rats with diabetes insipidus (D.I.) would have significantly less medullary and papillary sodium than normal rats of the same strain, and that this deficiency might be corrected when D.I. rats are treated with vasopressin. The first series of experiments was designed to test these predictions. Disagreement also persists on the effect of dehydration on the composition of the renal medulla and papilla. At least two groups of investigators found sequestration of papillary sodium to be greater in hydropenic dogs than in dogs in water diuresis (2, 7). Jaenike's studies suggested that there was no difference (3). Saikia (8), on the other hand, reported the medullary content of sodium to be significantly greater in hydropenic than in water-loaded hamsters, but he could …

the journal of clinical investigation/the journal of clinical investigation

Sequestration of urea and nonurea solutes in renal tissues of rats with hereditary hypothalamic diabetes insipidus: effect of vasopressin and dehydration on the countercurrent mechanism.