Identification and characterization of a ouabain-like compound from human plasma.
- J. Hamlyn, M. Blaustein, J. H. Ludens
- BiologyProceedings of the National Academy of Sciences…
- 15 July 1991
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.
- M. Blaustein, F. Leenen, W. Wier
- BiologyAmerican Journal of Physiology. Heart and…
- 1 March 2012
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.
- A. Arnon, J. Hamlyn, M. Blaustein
- BiologyAmerican Journal of Physiology - Cell Physiology
- 2000
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(+).
- A. Arnon, J. Hamlyn, M. Blaustein
- BiologyAmerican Journal of Physiology. Heart and…
- 1 August 2000
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.
Activation of c-SRC underlies the differential effects of ouabain and digoxin on Ca(2+) signaling in arterial smooth muscle cells.
- A. Zulian, Cristina I. Linde, V. Golovina
- BiologyAmerican Journal of Physiology - Cell Physiology
- 15 February 2013
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.
- Jin Zhang, M. Lee, M. Blaustein
- Biology, MedicineJournal of Physiology
- 2005
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.
Long-term ouabain administration produces hypertension in rats.
- C. Yuan, P. Manunta, M. Pamnani
- Biology, MedicineHYPERTENSION
- 1 August 1993
Ouabain, given chronically, is associated with the development of hypertension in RRM rats as well as in normal rats, and was greater in animals with greater degrees of RRM for a given ouabains dose.
The Pump, the Exchanger, and Endogenous Ouabain: Signaling Mechanisms That Link Salt Retention to Hypertension
- M. Blaustein, Jin Zhang, J. Hamlyn
- BiologyHYPERTENSION
- 1 February 2009
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.
Salt intake and depletion increase circulating levels of endogenous ouabain in normal men.
- P. Manunta, B. Hamilton, J. Hamlyn
- Medicine, BiologyAmerican Journal of Physiology. Regulatory…
- 1 March 2006
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.
Chronic hypertension induced by ouabain but not digoxin in the rat: antihypertensive effect of digoxin and digitoxin.
- P. Manunta, J. Hamilton, A. Rogowski, B. Hamilton, J. Hamlyn
- Biology, MedicineHypertension Research
- 1 September 2000
It is suggested that sodium pump inhibition is not the exclusive mediator of the hemodynamic effects of these cardiac glycosides and the presence of structure-specific mechanisms that regulate their tissue levels and effects on long-term blood pressure is demonstrated.
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