The relation of a circulating sodium transport inhibitor (the natriuretic hormone?) to hypertension

It is proposed that in essential hypertension the underlying genetic lesion is a renal difficulty in excreting sodium, which becomes more apparent the higher the sodium intake. It is further proposed that the renal lesion is the cause of the observed rise in the plasma's capacity to inhibit Na+...

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Bibliographic Details
Published in:Medicine (Baltimore) 1983-09, Vol.62 (5), p.310-326
Main Authors: de Wardener, H E, MacGregor, G A
Format: Article
Language:English
Subjects:
Animals
Biological Transport, Active
Dogs
Enzyme Induction
Erythrocytes - metabolism
Glucosephosphate Dehydrogenase - biosynthesis
Guinea Pigs
Humans
Hypertension - etiology
Hypertension - genetics
Kidney Failure, Chronic - physiopathology
Muscle Tonus
Muscle, Smooth - physiology
Natriuresis
Natriuretic Agents
Peptides
Proteins - physiology
Rats
Sodium - antagonists & inhibitors
Sodium - metabolism
Sodium - physiology
Sodium-Potassium-Exchanging ATPase - antagonists & inhibitors
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Summary:It is proposed that in essential hypertension the underlying genetic lesion is a renal difficulty in excreting sodium, which becomes more apparent the higher the sodium intake. It is further proposed that the renal lesion is the cause of the observed rise in the plasma's capacity to inhibit Na+-K+-ATPase and that the inhibitor's action on vascular smooth muscle eventually leads to the rise in blood pressure.
ISSN:0025-7974
1536-5964
DOI:10.1097/00005792-198309000-00004