J E Sealey
Albert Einstein College of Medicine
20 Papers
164 Citations
J E Sealey is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Renin–angiotensin system & Plasma renin activity. The author has an hindex of 10, co-authored 20 publications.
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Papers
Low Urinary Sodium Is Associated With Greater Risk of Myocardial Infarction Among Treated Hypertensive Men
TL;DR: Myocardial infarction and UNaV were inversely associated in the total population and in men but not in women, who sustained only nine events, and no association was observed between non-cardiovascular disease mortality andUNaV.
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Interruption of the renin-angiotensin system in hypertensive patients by captopril induces sustained reduction in aldosterone secretion, potassium retention and natruiresis.
TL;DR: The observed effects on aldosterone and electrolyte balance strongly suggest that inhibition of angiotensin converting enzyme in vivo produces a sustained reduction in biologically active angiotENSin II levels.
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•Journal Article
Renin relationship to sex, race and age in a normotensive population.
Gary D. James,J E Sealey,Franco B. Muller,Michael H. Alderman,Shantha Madhavan,John H. Laragh +5 more
TL;DR: It is suggested that renin activity tends to be lower in older subjects and that differences in reninActivity related to sex and race, while statistically significant, may not be physiologically important.
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Activation of a prorenin-like substance in human plasma by trypsin and by urinary kallikrein.
TL;DR: Using maximum trypsin activation to define “total” renin, it is found that among 22 normal subjects and hypertensive patients there was a direct relationship between the proportion of active renin in plasma (active/ total) and the concurrent urinary kallikrein excretion (r = 0.46, p < 0.05), suggesting that there might be a link between prorenin and renal kallIKrein in vivo.
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Detection and isolation of inactive, large molecular weight renin in human kidney and plasma.
TL;DR: Both human plasma and kidney contain an inactive, prorenin-like substance that can be detected reliably by trypsin activation, and the similarity of other characteristics suggests that these substances may be one and the same substance.
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