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Identification and characterization of a ouabain-like compound from human plasma.
TLDR
An endogenous substance from human plasma is purified and structurally identified by mass spectroscopy that binds with high affinity to this receptor and that is indistinguishable from the cardenolide ouabain.
How NaCl raises blood pressure: a new paradigm for the pathogenesis of salt-dependent hypertension.
TLDR
Recent evidence is summarized that defines specific molecular links between Na(+) and the elevated vascular resistance that directly produces high BP, and several central and peripheral mechanisms are coordinated by EO to effect and maintain the salt-induced elevation of BP.
Na(+) entry via store-operated channels modulates Ca(2+) signaling in arterial myocytes.
TLDR
It is demonstrated that the SOC are a major Na(+) entry route in arterial myocytes and has unexpectedly large effects on cell-wide Ca(2+) signaling.
Ouabain augments Ca(2+) transients in arterial smooth muscle without raising cytosolic Na(+).
TLDR
Results suggest that Na(+) enters a tiny cytosolic space between the plasmalemma (PL) and the adjacent sarcoplasmic reticulum (SR) via an Mg(2+)- and La(3+)-blockable mechanism that is activated by SR store depletion.
Salt intake and depletion increase circulating levels of endogenous ouabain in normal men.
TLDR
The dramatic impact of high-salt diets on plasma EO is consistent with its proposed role as a humoral vasoconstrictor that links salt intake with vascular function in hypertension.
Activation of c-SRC underlies the differential effects of ouabain and digoxin on Ca(2+) signaling in arterial smooth muscle cells.
TLDR
In contrast to ouabain, the interaction of digoxin with α2 Na(+) pumps is unable to activate c-Src phosphorylation and upregulate the downstream NCX1-TRPC6 Ca(2+) signaling pathway in ASMCs, which may underlie its inability to raise long-term BP.
Sodium pump alpha2 subunits control myogenic tone and blood pressure in mice.
TLDR
Ch chronically reduced alpha2 activity or chronic ouabain apparently regulates myogenic tone and long-term blood pressure whereas reduced alpha1 activity plays no persistent role: the in vivo changes in blood pressure reflect the in vitro changes in myogenictone.
Endogenous ouabain, sodium balance and blood pressure: a review and a hypothesis.
TLDR
Investigations of the efferent pressor mechanisms and the renal handling of endogenous ouabain are novel approaches to the etiology and therapy of several common cardiovascular disorders.
Angiotensin II stimulates secretion of endogenous ouabain from bovine adrenocortical cells via angiotensin type 2 receptors.
TLDR
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.
The Pump, the Exchanger, and Endogenous Ouabain: Signaling Mechanisms That Link Salt Retention to Hypertension
TLDR
The evidence is examined that endogenous ouabain (EO), Na+ pumps (Na,K-ATPase), and the Na/Ca exchanger (NCX) are critical molecular mechanisms in this pathway of NaCl retention and blood pressure (BP) elevation.
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