A circulating inhibitor of (Na+ + K+) ATPase associated with essential hypertension

John M. Hamlyn, Richard Ringel, Juergen Schaeffer, Paul D. Levinson, Bruce P. Hamilton, A. Avinoam Kowarski, Mordecai P. Blaustein

Research output: Contribution to journalArticlepeer-review


The aetiology of essential hypertension, a disease prevalent in cultured societies, is unknown. However, much evidence suggests that abnormal sodium metabolism has a critical role - This has led to the hypothesis that an increase in the circulating concentration of an inhibitor of (Na+ + K +) ATPase is responsible for the increased peripheral vascular resistance in essential hypertension1. Evidence for relatively high levels of a Na+ pump inhibitor in essential hypertension has come from bioassay and cytochemical assays of plasma and urine from normotensive and hypertensive individuals2,3. There is also evidence for increased plasma levels of a Na+ pump inhibitor in some animal models (for example, renal and deoxycorticosterone acetate (DOCA) models) of hypertension4. Nevertheless, direct biochemical determination of (Na+ + K+) ATPase inhibition by this substance has not yet been reported. We demonstrate here, with a kinetic (Na+ + K +) ATPase assay, a highly significant correlation between levels of a plasma inhibitor of (Na+ + K+)ATPase activity and mean arterial blood pressure (MAP) in normotensive and hypertensive individuals. These data provide evidence for the involvement of a circulating Na+ pump inhibitor in the genesis of essential hypertension. Moreover, our assay methods may be useful for the isolation and characterization of this inhibitor.

Original languageEnglish (US)
Pages (from-to)650-652
Number of pages3
Issue number5893
StatePublished - 1982
Externally publishedYes

ASJC Scopus subject areas

  • General


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