Familial abnormality of erythrocyte cation transport in essential hypertension.

Abstract

phages was still five times greater than control numbers and this could have been related to lack of complete recovery in permeability, which we found in our subjects after stopping smoking. We have not found a relation between amount smoked and the change in number of alveolar macrophages, and it would be interesting to compare the result of such a study with our finding of a relation between carboxyhaemoglobin and half-time clearance.The large change in the results of the permeability test and lack of effect on tests of ventilatory function are noteworthy. This implies that the alveolar permeability to the tracer 99mTc-DTPA is a very sensitive test of pulmonary dysfunction in cigarette smokers and the results are correlated with exposure to tobacco smoke. During the 21 days after stopping smoking recovery into the normal non-smoking range was the exception, and the greatest degree of recovery occurred in those with least exposure to tobacco smoke. Cation transport across the red-cell membrane was studied in subjects with essential hypertension and their relatives using rubidium-86 as an analogue of potassium. The activity of the ouabain-sensitive sodium-potassium pump was significantly greater in patients with untreated essential hypertension than in controls (p <0 001). No clear separation was seen between normotensive and hypertensive subjects. Activity of the sodium-potassium pump was also increased in a proportion of normotensive relatives of subjects with essential hypertension. Rubidium uptake was significantly lower in normotensive black subjects than in normotensive whites, the difference being in a ouabain-resistant pathway of cation transport. These results provide further evidence that a defect in membrane cation transport contributes to the pathogenesis of essential hypertension.

Race and sex differences in erythrocyte Na+, K+, and Na+-K+-adenosine triphosphatase.

“…The elevated RBC Na' concentration in the black group could result from a higher membrane permeability for this cation, a possibility that seems unlikely since other reports did not show such a phenomenon (16,36,37). Another cause for the racial differences in the intracellular Na+ concentration could be an altered activity of Na',K+-cotransport (16,17).…”

Evidence of a shared mechanism of vasoconstriction in pulmonary and systemic circulation in hypertension: a possible role of intracellular calcium.

“…Several investigators have described a defect in ion transport across the erythrocyte membrane in animal hypertension,'0 as well as in red' -14 and white blood cells'5 of patients with essential hypertension or of their normotensive offspring. 16 17 Impairment of the sodium pump has been found by some workers,'5 and a deficiency in the Na+/K+ cotransport system has been described by others."' As related to hypertension, these disorders are spread throughout the body and involve arteriolar smooth muscle, which is the actual culprit.…”

Plasma digitalislike activity in essential hypertension or end-stage renal disease.

“…These changes include an increase in intracellular Na + ," an increase in the net Na + efflux from erythrocytes, 20 and a reduction of leukocyte Na + effluxes in the absence 21 or presence of plasma. 22 The presence of an endogenous inhibitor in normotensive subjects with a family history of hypertension indicates either a genetic transmission or some peculiar environmental influence.…”