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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Net sodium (Na) efflux and potassium (K) influx were determined in Na-loaded/K-depleted erythrocytes derived from 37 patients with essential hypertension and 25 age-matched normotensive subjects with no family history of hypertension, together with the measurement of basal red cell sodium and potassium contents. Intraerythrocyte sodium content was significantly higher in the essential hypertensives than in the normotensives (10.9 +/- 1.4 vs 10.0 +/- 1.2 mmol/L X cells, mean +/- SD, p less than 0.02), but potassium content was nearly equal between the two groups. Net Na efflux in the hypertensives was significantly reduced compared with that in the normotensives (4.57 +/- 0.70 vs 5.18 +/- 1.02 mmol/L X cells X hr, p less than 0.01), but both net K influx and net Na/K flux ratio were not significantly different between the two groups. Net Na efflux and K influx showed a significant inverse correlation with red cell sodium content (r = -0.64 and r = -0.56, respectively, p less than 0.001). These results suggest that the reduced net Na efflux with the increase of red cell sodium content may be related to the pathogenesis of essential hypertension. However, it is impossible to determine the genetic marker of essential hypertension by using the net Na/K flux ratio of Japanese subjects, although Garay et al. have reported that this index was abnormally low in the case of Europeans.
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PMID:Abnormal red cell sodium content and efflux in Japanese patients with essential hypertension. 609 Jul 19

The Na+ content of erythrocytes is elevated in people with essential hypertension. There is conflicting evidence about its cause. The present study was designed to investigate whether the increase in content is due to a defect in a ouabain-resistant Na+ flux. Net Na+ influx was determined from the increase in Na+ content of erythrocytes during incubation in the presence of ouabain. Na+ content of erythrocytes from 24 normotensive Caucasian subjects with no known family history of hypertension was 6.9 +/- 1.3 mmol per litre of cells. It was 7.9 +/- 2.0 mmol per litre of cells in 18 subjects with essential hypertension. The difference was less and not significant when the two non-Caucasian subjects of the hypertensive group were excluded. Net Na+ influx was 1.83 mmol/h per litre of cells in the normotensive group. In eight subjects it was measured on a second occasion after an interval of several months. The coefficient of a variation of the duplicate tests was 2.4%. Net Na+ influx was significantly higher in the hypertensive group, the value was 2.18 +/- 0.15 mmol/h per litre of cells. In 11 of these subjects, Na+ influx was measured on a second occasion. The coefficient of variation was 6.2%, significantly greater than in the control group. In some of these subjects Na+ influx was within the normal range on one of the two occasions. When the groups were compared with use of the mean values from the duplicate tests, net Na+ influx was elevated in 17 of the 18 hypertensive subjects. The findings are discussed with reference to previous work and in relation to the established facilitatory effects of an increased intracellular Na+ concentration on excitable cells that influence blood pressure.
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PMID:Ouabain-insensitive net sodium influx in erythrocytes of normotensive and essential hypertensive humans. 613 24

Net Na+ and K+ fluxes were measured in Na+-loaded and K+-depleted erythrocytes of three varieties of genetically hypertensive rats. In Okamoto spontaneously hypertensive rats (4 and 10-12 weeks of age), Na+ extrusion was reduced as compared to normotensive controls (Wistar/Kyoto). Na+ extrusion was also reduced in the hypertension-prone substrain of the Hebrew University Sabra rats as compared to the Na+-resistant substrain. K+ fluxes were similar in both groups. In both Okamoto spontaneously hypertensive rats and the hypertension-prone substrain, hypertension was severe and developed rapidly. In the Lyon spontaneously hypertensive rats, in which the blood pressure elevation is less severe than in other genetically hypertensive rats, erythrocyte net Na+ extrusion was the same as in normotensive controls, but net K+ gain was slightly increased. These erythrocyte abnormalities, observed in three varieties of genetically transmitted hypertension of the rat, are in several aspects similar to those previously described in accelerated and benign human essential hypertension. Erythrocyte Na+ and K+ net flux alterations may thus represent biochemical markers of primary hypertension.
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PMID:Abnormal net Na+ and K+ fluxes in erythrocytes of three varieties of genetically hypertensive rats. 625 18

Various parameters of erythrocyte membrane sodium transport were measured in patients with untreated essential hypertension, in the normotensive offspring of parents with hypertension, and in patients whose hypertension had been controlled by medication. Net sodium efflux, measured by an isotopic tracer technique, was 2.12 +/- 0.17 mM Na+/1 of red blood cells (RBCs)/hr in patients with untreated essential hypertension, compared with 1.55 +/- 0.12 mM Na/1 of RBCs/hr in a group of normotensive controls (p less than .025). Partitioning sodium efflux into ouabain-sensitive and ouabain-insensitive components revealed a significant elevation of both components of membrane sodium transport in the patients with untreated essential hypertension. Ouabain-sensitive sodium efflux was 1.38 +/- 0.09 mM Na/1 RBCs/hr in the patients, compared with 1.04 +/- 0.07 mM Na/1 RBCs/hr in the controls. Ouabain-insensitive sodium efflux was also increased from 0.51 +/- 0.05 mM Na/1 RBCs/hr in the controls to 0.74 +/- 0.09 mM Na/1 RBCs/hr in those with untreated hypertension. Despite these changes in sodium efflux, Na,K-ATPase activity in the erythrocyte membrane, measured at maximum velocity (Vmax), was normal, suggesting that the observed abnormalities in membrane sodium transport in patients with untreated essential hypertension resulted from a change in pump control mechanisms rather than a change in enzyme activity. With the techniques used in this study we were unable to identify changes in erythrocyte membrane transport in the normotensive offspring of hypertensive parents. Membrane sodium transport was also examined in hypertensive patients whose blood pressure had been controlled by medication. In this group it was found that erythrocyte sodium transport did not differ from that in our control group, which suggests that treatment of hypertension can modify fundamental pathophysiologic changes at the level of the cell membrane.
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PMID:Erythrocyte membrane sodium transport in patients with treated and untreated essential hypertension. 630 25

Net fluxes of sodium and potassium ions were determined in sodium-loaded, potassium-depleted erythrocytes from 370 white subjects, 194 of whom had essential hypertension or had been born to parents with essential hypertension. Findings were compared with those in 86 controls who were normotensive and did not have a family history of hypertension. Compared with controls all patients with essential hypertension had a low sodium to potassium ratio secondary to a deficit in the sodium-potassium cotransport system. A similar abnormality was found in subjects born to parents with essential hypertension, the prevalences of a deficient cotransport system in such subjects being 53.6% (52 out of 97) among those with one hypertensive parent and 73.7% (14 out of 19) among those with two hypertensive parents. Both sexes were equally affected. Studies in 14 families over two or three generations showed the erythrocyte cation abnormality in one or more members of each consecutive generation. No close association was evident between the deficient erythrocyte sodium-potassium cotransport system and either blood groups ABO, Rh, Kidd, Duffy, P, and MNS or the major histocompatibility HLA antigens. Out of 90 consecutive unrelated and normotensive white blood donors, 36 showed a low erythrocyte sodium-potassium net flux ratio. It is concluded that in white people abnormal erythrocyte cation transport is a biochemical disorder characteristic of essential hypertension and transmitted by a dominant and autosomal mode expressing a single abnormal gene.
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PMID:Inheritance of abnormal erythrocyte cation transport in essential hypertension. 678 58