Search PubMed⌕ Search

Biomedical subjects

H Losse

Publications and source records attributed to H Losse.

At least 55 records · Page 3Linked to original sources
PubMed1983

Sodium and calcium in lymphocytes and erythrocytes in essential hypertension.

The present study compared protein-related sodium concentrations in lymphocytes with the sodium and calcium activities in erythrocytes from 12 untreated patients with essential hypertension and 15 normal control subjects. It appeared that protein-related Na+ in lymphocytes was elevated about threefold in essential hypertensives. Comparable increases were also noted in intracellular Na+ and Ca2+ activities. The correlation between Na+ in lymphocytes and in erythrocytes was not close. These results suggest that the determination of protein-related Na+ in lymphocytes discriminates between normotensives and essential hypertensives as well as measurements of ion activities in erythrocytes. Altered intracellular ion binding may be partly responsible for the changes in intracellular protein-related Na+.

Calcium↗
PubMed1982

[Intracellular electrolytes and serum lipids in relation to dietary fatty acid intake].

In 12 moderately obese female probands without metabolic abnormalities, intracellular Mg++ activity, Na+ activity and Na+ concentration, and serum triglycerides, total cholesterol and HDL cholesterol were measured under a diet with fatty acids varying in the degree of saturation. During the diet with mainly saturated fatty acids the intracellular Na+ activity and concentration fell from 7.34 +/- 2.02 to 6.37 +/- 1.43 (p less than 0.05) and from 5.28 +/- 0.57 to 4.98 +/- 0.80 mmol/l respectively (mean values +/- SD). Intracellular Mg++ activity fell from 1.36 +/- 0.23 to 1.20 +/- 0.17 mmol/l (p less than 0.05). During the subsequent diet consisting of mainly polyunsaturated fatty acids, intracellular Na+ activity and concentration rose to 7.95 +/- 2.81 and 5.17 +/- 0.91 mmol/l respectively (p less than 0.05). The intracellular Mg++ activity showed a further decrease to 1.04 +/- 0.14 mmol/l (p less than 0.01). During the diet consisting of mainly saturated fatty acids there was a significant correlation between the changes in HDL cholesterol and intracellular Na+ activity (r = -0,78; p less than 0.01). The initial values of intracellular Mg++ correlated with HDL cholesterol (r = 0.53; p less than 0.05). Thus, moderate obesity at any rate was not associated with intracellular electrolyte disturbances. The composition of dietary fatty acids affects intracellular electrolyte composition. This may be caused on the one hand by modified membrane function due to the uptake of the various fatty acids into the membrane, and on the other hand by changes in the synthesis of prostaglandins depending on the intake of precursors.

Adult↗
PubMed1982

Intracellular sodium and calcium in essential 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.

Adolescent↗
PubMed1982

Intracellular Na+ and Ca2+ activities in aortic smooth muscle cells from spontaneously hypertensive rats.

Elevations of intracellular Na+ and Ca2+ in essential hypertension have up to now only been demonstrated in blood cells. Therefore, intracellular Na+ and Ca2+ activities were determined in cultured aortic smooth muscle cells from nine spontaneously hypertensive rats of the Münster strain and from nine normotensive Wistar rats. Intracellular ion activities were determined by ion-selective electrodes. In muscle cells from spontaneously hypertensive rats intracellular Na+ activity was markedly elevated (P less than 0.01), whereas intracellular Ca2+ was not significantly different. This points to the preponderance of genetic causes for the elevation of intracellular Na+, whereas the disturbances in cellular Ca2+ metabolism may additionally require humoral factors to become manifest.

Animals↗
PubMed1982

Effect of nifedipine on blood pressure and on intracellular calcium in arterial hypertension.

In 13 patients with essential and renal hypertension, the influence of nifedipine on the intracellular free Ca2+ concentration was tested. Measurements of free Ca2+ were performed with a Ca2+ -selective electrode. The patients were additionally treated with a conventional antihypertensive combination therapy, by which the blood pressure could not be lowered satisfactorily. Under treatment with 30-60 mg of nifedipine daily, blood pressure was lowered from 192 +/- 23/95 +/- 15 mm Hg to 147 +/- 20/83 +/- 16 mm Hg. The intracellular Ca2+ activity fell from 7,115 +/- 14,139 to 1,886 +/- 3,748 mumol/L (p less than 0.05). The decrease in intracellular Ca2+ correlated very well with the initial value of Ca2+ activity (r = 0.966); furthermore, a relationship was found with the serum creatinine level (r = 0.48). On the other hand, there was no correlation with the decrease in blood pressure. In the lower dose range, nifedipine did not elicit a clear reduction in intracellular Ca2+. The results show that intracellular Ca2+ activity can be influenced by Ca2+ antagonists, but that there is no direct relationship between intracellular free calcium and blood pressure.

Adult↗
PubMed1981

[Intracellular sodium and calcium as a genetic marker in essential hypertension].

In 33 normotensive probands with a familial disposition to hypertension and in 18 normotensives without a family history of hypertension, aged 15 to 24 years, intracellular Na+ and Ca2+ activity in red blood cells was determined by ion-selective electrodes. The activities represent the free, i.e. unbound intracellular fraction of each ion. In the group with a family history of hypertension the mean intracellular Na+ activity was 9.74 +/- 1.43 mmol/l and clearly exceeded that in the group without predisposition to hypertension, which was 7.74 +/- 1.06 mmol/l. Even larger differences were found in mean intracellular Ca2+ activity (9.54 +/- 9.56 mumol/l in the group with familial disposition and 1.87 +/- 3.47 mumol/l in the control group). However, due to the relatively wide range of the values, especially with respect to the Ca2+ activities in probands with familial disposition to hypertension, the values from the two groups overlapped. The results suggest that elevation of intracellular Na+ and Ca2+ activity may be evidence for a genetically determined later development of hypertension.

Adolescent↗
PubMed1981

Monoclonal gammopathies in Sézary syndrome: a report of four new cases and a review of the literature.

Clinical and laboratory findings of four patients with Sézary syndrome and monoclonal gammopathy are presented. In the literature five cases with the association of these symptoms have been reported. Among the authors' series of 13 patients with Sézary syndrome, monoclonal gammopathy was observed far more often than could be expected from its natural incidence. It appears likely that monoclonal gammopathy is related to Sézary syndrome.

Aged↗
PubMed1981

Intracellular cation activities and concentrations in spontaneously hypertensive and normotensive rats.

1. The intracellular concentrations of Na+,K+ and Ca2+ were measured in the erythrocytes of spontaneously hypertensive rats and normotensive Wistar rats. 2. The intracellular Na+ concentration in hypertensive rats was slightly elevated at 3.16 +/- 0.25 compared with 2.85 +/- 0.35 mmol/l (P approximately 0.05) and intracellular Na+ activity was markedly increased in hypertensive rats. 3. Intracellular Ca2+ activity was 7519 +/- 28990 nmol/l of free water in hypertensive rats compared with 123 +/- 98 in controls (P less than 0.01). 4. The cytoplasm of hypertensive animals did not buffer Ca2+ as effectively as that of normal animals. 5. It is concluded that a decreased binding capacity of intracellular macromolecules for Na+ and Ca2+ may explain the disturbances of intracellular electrolyte composition in spontaneously hypertensive rats.

Animals↗
PubMed1981

Intracellular Na+ as a genetic marker of essential hypertension.

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.

Animals↗
PubMed1981

[Disturbed sodium and calcium exchange in erythrocytes of spontaneously hypertensive rats (author's transl)].

In red blood cells of spontaneously hypertensive and of normotensive rats intracellular NA+ activity (a(i)Na), Na+ concentration (]Na+]i) and Ca2+ activity (a(i)Ca) were measured by ion-selective electrodes and flame photometry, respectively. In spontaneously hypertensive rats a(i)Na and a(i)Ca were significantly elevated as compared with the normotensive controls, whereas [Na+]i showed no significant difference. In hypertensive animals a(i)Na, exceeded [Na+]i, in normotensive rats a(i)Na was lower than [Naf+]i. From these results it can be concluded: (1) In spontaneously hypertensive rats the transmembraneous distribution of free Na+ is altered, (2) an elevation of intracellular free Ca2+ may contribute to increased vascular contractility in hypertensive animals, (3) the described abnormalities may be caused by a lowered binding-capacity of intracellular macromolecules for Na+ and Ca2+.

Animals↗