Cited by 309
Charing Cross Hospital
Publishes on Ion Transport and Channel Regulation, Electrolyte and hormonal disorders, Renal function and acid-base balance. 36 papers and 1.8k citations.
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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.
1. Eight patients with chronic renal failure (creatinine clearance 4·9–22·0 ml/min) were given 75–150 ml of aluminium hydroxide gel (‘Aludrox’) daily for 20–32 days. 2. In all patients there was a decrease in plasma phosphorus. The phosphorus balance became more negative in four and less positive in one, remained unchanged in two, and became positive in one. 3. Patients absorbed 100–568 mg of aluminium daily. In two of three patients the content of aluminium in the iliac bone increased but not above normal values. 4. The concentration of parathyroid hormone was decreased by aluminium hydroxide therapy in three patients in whom there was an increase in plasma calcium and in one other patient in whom plasma calcium did not change.
1. Two normal subjects and ten patients with chronic renal failure were given 15 or 20 g of calcium carbonate in the morning and 5·6 or 8·4 g of calcium phosphate in the evening for 13–41 days. 2. During the high calcium and phosphate intake there was a rise in calcium and phosphate absorption from the gut in the normal subjects and to about the same extent in the patients with chronic renal failure. 3. The calcium and phosphate balances became positive while there was a rise in plasma calcium and a fall in plasma phosphate. There was also a fall in urinary phosphate excretion.