Evidence for a circulating sodium transport inhibitor in essential hypertension.

Lucilla Poston(Charing Cross Hospital), R. B. Sewell(King's College Hospital), S P Wilkinson(Mayo Clinic in Florida), P J Richardson(King's College Hospital), Rebecca Williams(Mayo Clinic in Florida), E. M. Clarkson(Mayo Clinic in Florida), Graham A. MacGregor(Mayo Clinic in Florida), H. E. de Wardener(Charing Cross Hospital)
BMJ
March 14, 1981
Cited by 289Open Access
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Abstract

The active sodium transport of white cells and red cells obtained from patients with essential hypertension was impaired. Incubating white cells from normotensive subjects in serum obtained from patients with essential hypertension caused an impairment in sodium transport in the white cells of normotensive subjects similar to that found in the white cells of hypertensive patients. The impairment in sodium transport was due to a fall in the ouabain-sensitive component of the total sodium efflux rate constant. These results show that the serum of patients with essential hypertension contains a substance which influences sodium transport and that it has ouabain-like activity. They also suggest that it is this substance which causes the impairment in sodium transport in the leucocytes of patients with essential hypertension. These findings support the hypothesis that the rise in blood pressure in patients with essential hypertension is due to an increased concentration of a circulating sodium transport inhibitor which is continuously correcting a tendency for sodium retention by the kidney.


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