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Jui R. Shah

Researcher at University of Maryland, Baltimore

Publications -  5
Citations -  365

Jui R. Shah is an academic researcher from University of Maryland, Baltimore. The author has contributed to research in topics: Adrenal cortex & Ouabain. The author has an hindex of 5, co-authored 5 publications receiving 358 citations.

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Angiotensin II Stimulates Secretion of Endogenous Ouabain From Bovine Adrenocortical Cells via Angiotensin Type 2 Receptors

TL;DR: The results demonstrate that AT2 receptors stimulate secretion of endogenous ouabain from bovine adrenocortical cells and indicates that separate signaling mechanisms having minimal cross talk control the adrenoc Cortical secretions of corticosteroids and cardiac-active steroids.
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Observations on the Nature, Biosynthesis, Secretion and Significance of Endogenous Ouabain

TL;DR: It is suggested that at least one of the mammalian counterparts to the cardiac glycosides is a novel steroidal isomer of ouabain, which is secreted by the adrenal cortex, and augments cardiovascular function.
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11-hydroxylation in the biosynthesis of endogenous ouabain: multiple implications.

TL;DR: Accumulating evidence indicates that mammals use steroidal glycosides with ‘digitalis‐like’ activity and the existence of an additional ring in the hemiketals raises the possibility that their in vivo physiological targets and actions differ from the isolated form of EO.
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Different Signaling Pathways Mediate Stimulated Secretions Of Endogenous Ouabain and Aldosterone From Bovine Adrenocortical Cells

TL;DR: The results show that the secretions of aldosterone and endogenous ouabain from bovine adrenocortical cells are mediated by different intracellular signaling mechanisms and provide evidence that the adrenalsecretions of these steroids are regulated differently.
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Synaptic plasticity in sympathetic ganglia from acquired and inherited forms of ouabain-dependent hypertension.

TL;DR: The results favor the possibility that enhanced duration of LTP in sympathetic neurons contributes to the increase in sympathetic nerve activity in ouabain-dependent hypertension and suggest that a captopril-sensitive step mediates the link of ouABain with LTP.