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

In normal subjects, the rate of aldosterone secretion fluctuates widely according to the state of salt and water balance, but the pathways mediating this relationship are still to be identified. Hypersecretion of aldosterone occurs in malignant nephrosclerosis (2). Angiotensin, the pressor peptide released from plasma by renin, increases both the adrenal secretion (3) and the urinary excretion (4) of aldosterone in man. These observations support the suggestion (5) that a renaladrenal interaction might be involved in the normal regulation of sodium and potassium balance. By this mechanism, the kidney, perhaps sensitive to diminished arterial filling or ischemia, secretes renin, generating angiotensin, which then stimulates aldosterone secretion. Aldosterone, in turn, restores renal perfusion by promoting sodium and water retention. In malignant hypertension this mechanism may become deranged, leading to the coexistence of increased amounts of both angiotensin and aldosterone in the blood, a possibility that derives additional support from the earlier report (6) of increased blood angiotensin in these patients. On the other hand, since neither renin nor angiotensin has been conclusively demonstrated in normal human plasma, elaboration of these substances in malignant hypertension might be simply a consequence of severe renal damage. Our more recent work has investigated the possibility that this renal-adrenal interaction participates in normal homeostasis, as well as in the

ANGIOTENSIN II, NOREPINEPHRINE, AND RENAL TRANSPORT OF ELECTROLYTES AND WATER IN NORMAL MAN AND IN CIRRHOSIS WITH ASCITES*