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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.

In 1960 the pathophysiological mechanisms by which Na+ is involved in human essential hypertension were first elucidated by the finding that intracellular Na+ is elevated in red blood cells of essential hypertensives. Furthermore it was found that (1) transmembranous Na+ fluxes in red blood cells of essential hypertensives are changed in parallel with intracellular Na+ concentration, reflecting the metabolic disturbances better than the Na+ concentration measurements, (2) in normotensives with a familial disposition of essential hypertension intracellular Na+ and transmembranous Na+ fluxes are elevated, (3) uremia affects intracellular Na+ levels similarly as essential hypertension, and (4) intracellular free Na+ and free Ca++ is increased in spontaneously hypertensive rats. It can be assumed that elevated intracellular Na+ plays a causative role in essential hypertension.

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In 14 hypertensives the effect of captopril (angiotensin-converting enzyme inhibitor) treatment on red blood cell Na+, K+, Mg2+ and Zn2+ concentrations and on plasma Zn2+ concentrations were studied. Intraerythrocytic Zn2+ concentrations increased slightly, whereas plasma zinc concentrations decreased. The concurrence of hypozincemia with side effects resembling the symptoms of zinc deficiency such as loss of smell and taste suggests a role of alterations in zinc metabolism for the pharmacodynamics of captopril.

In order to examine the role of humoral factors for the development of hypertension in the spontaneously hypertensive rat of the Münster strain (SHR) cross circulation experiments with normotensive Wistar Kyoto rats were performed. Cross circulation between SHR and normotensive rats for 30 min increased mean arterial pressure in the latter by 29.1 +/- 7.6 mm Hg (p less than 0.01). Transmission of hypertension by cross circulation was abolished by nephrectomy, adrenalectomy, volume depletion or chronic salt restriction in the SHR. It is concluded that hypertension in SHR is caused by a circulating hypertensive agent produced in kidneys and adrenals, the secretion of which can be suppressed by volume or salt depletion.

In aortic smooth muscle cells from spontaneously hypertensive and normotensive rats, which were separated from the blood vessels by enzymatic digestion, intracellular Na+ and Ca2+ activities were measured. The determinations were made by ion-selective electrodes. In smooth muscle cells from spontaneously hypertensive rats intracellular Na+ and Ca2+ activities were elevated as compared to cells from normotensive rats (P less than 0.001 for Na+ and P less than 0.01 for Ca2+). Since in cultured aortic smooth muscle cells from spontaneously hypertensive rats intracellular Ca2+ is known to be not significantly increased, primarily humoral factors may account for the changes in intracellular Ca2+ reported.