The intracellular Na+ and Ca2+ activity andNa+ concentration were measured in erythrocytes of normotensive subjects, with and without a familial disposition to hypertension, in essential hypertensive patients with and without a family history of hypertension, and in patients with secondary hypertension. 2.In normotensive subjects without a genetic trait of hypertension intracellular Na+ activity and concentration were 7-00 L-1.38 mmol/l and 5.67 f 0.95 mmol/l respectively. The intracellular Ca2+ activity was 4.82 & 4-49 Nmol/l. In normotensive subjects with a familial hypertensive disposition intracellular Na+ activity and concentration were 9.74 f 1-43 mmol/l (P < 0.01) and 6.63 f 0.88 mmol/l (P < 0.05). Intracellular Ca2+ was 9-59 f 9.71 pmolll (P < 3. Essential hypertensive patients without a familial genetic trait had an elevated intracellular Na+ activity (8.35 f 2.08 mmol/l, P < 0.05).Intracellular Na+ concentration was 6.64 f 0-79 mmol/l (P < 0.05). The intracellular CaZ+ activity was markedly elevated to 25.33 f 19.03 pmol/l (P < 0.01). The essential hypertensive patients with a familial disposition had an elevated intracellular Na+ activity (17.19 f 4.37 mmol/l, P < 0-001) and Ca2+ activity (32.8 f 32.51 pmol/l, P < 0.01). The intracellular Na+ concentration was 6.25 f 1-23 mmol/l. 4.The results indicate that in essential hypertension intracellular Na+ activity is increased, particularly in patients with a familial disposition for hypertension. Intracellular Ca2+ is increased in essential hypertension whether or not there was a family disposition to hypertension.
Intracellular sodium and calcium activities were measured by ion-selective electrodes in red blood cells of primary hypertensives and of normotensives with and without a familial disposition to hypertension. Intraerythrocytic sodium activity was markedly elevated in patients and normotensives with a familial disposition to hypertension (15.16 +/- 2.35 mmol/l in hypertensives and 9.74 +/- 1.43 mmol/l in normotensives, respectively, mean value +/- SD) as compared to the corresponding group without such a history (8.35 +/- 2.08 mmol/l in hypertensives and 7.00 +/- 1.38 mmol/l in normotensives). Mean intraerythrocytic calcium activity showed the highest values in patients with hypertension (32.8 +/- 32.5 mumol/l in patients with and 25.3 +/- 19.0 mumol/l in those without a familial disposition to hypertension), whereas in normotensives mean calcium activity was much lower (9.6 +/- 9.7 and 4.8 +/- 4.5 mumol/l, respectively). Our results document that a disturbed intraerythrocytic sodium metabolism is limited to patients with essential hypertension and a familial disposition to hypertension and, to a lesser extent, to normotensives showing a familial disposition to hypertension. Thus, a genetically determined alteration in intracellular sodium can be assumed. Furthermore, the observation of an enhanced intraerythrocytic calcium in some essential hypertensives with and without a familial disposition suggests additional factors, other than sodium, responsible for the disturbed intracellular calcium balance in these patients.
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