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  • 1
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Basal and stimulated TSH decreased progressively. Basal TSH was suppressed below the detection limit of 0.4 μU/ml after 74 h in 2 of the T3 and all of the T4 treated indiduals. At this time, in both groups 3 individuals could be significantly stimulated by TRH (about 5% of the pretreatment stimulation). There was no significant difference in the time course of suppression obtained by T3 or T4, though plasma T3 levels in the T4 treated group were considerably lower.
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  • 2
    ISSN: 0022-4731
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Keywords: Essential hypertension ; Erythrocytes ; Rubidium influx ; Na — K-cotransport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 86Rubidium influx and Na — K-cotransport have been investigated in erythrocytes of mild essential hypertensives and normotensives devoid of familial hypertension. For measurement of cotransport Na-loaded/K-depleted erythrocytes were used while rubidium influx (with and without ouabain) was determined under physiological conditions. Both transport systems were linear in time, the interassay variances in a range of about 10%. The patients with essential hypertension exhibited a decreased rubidium influx compared to the normotensive controls. Ouabain-sensitive fluxes were not significantly different between the two groups, whereas ouabain-resistent rubidium influx was diminished in the group of the patients. Na — K-cotransport was also found to be decreased in essential hypertension. There was no correlation between cotransport and Rb-influx. The results indicate changes in cation fluxes in erythrocytes of essential hypertensives, the Na — K-cotransport being rather more altered than rubidium influx. It is speculated that hypertensive persons with reduced rubidium flux rates may represent a subpopulation of essential hypertension and that their high blood pressure may be additionally influenced by exogeneous factors e.g. enhanced sodium uptake.
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  • 4
    ISSN: 1432-1440
    Keywords: Hyperthyroidism ; Erythrocytes ; Na-K ATPase ; Na-Li countertransport ; Intracellular sodium concentration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate the effect of thyroid hormones on erythrocyte cation transport systems and intracellular electrolyte content we have measured the activity of Na-K ATPase, Na-Li countertransport, as well as red cell sodium and potassium contents in patients with hyperthyroidism and in euthyroid controls. Intracellular Na- and K-concentrations were determined in erythrocytes washed three times in isotonic MgCl2 solution. Ouabain-sensitive Na-transport was estimated as the increase of Na before and after addition of ouabain in an erythrocyte suspension in isotonic Na-free medium. Na-Li countertransport was measured according to the method described by Canessa et al. [2]. The patients with hyperthyroidism exhibited a significantly elevated intracellular sodium content as well as a highly increased Na-K ATPase activity. Intracellular potassium content was not altered in the hyperthyroid subjects, but Na-Li countertransport was markedly decreased as compared to the controls. The results indicate that different ion transport systems of the erythrocyte membrane are influenced by thyroid hormones. We suggest that the elevation of Na-K ATPase activity might be due to the increased intracellular sodium concentration which is caused by the diminished countertransport pathway. Furthermore, the activity of Na-K ATPase, Na-Li countertransport, and intracellular sodium content in erythrocytes might be a useful peripheral indicator of thyroid hormone excess.
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  • 5
    ISSN: 1432-1440
    Keywords: Saralasin ; Angiotensin II ; Renin ; Rezeptoren ; Blutdruck ; Saralasin ; Angiotensin II ; Renin ; Receptors ; Blood pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary A modification of the infusion test with saralasin, an angiotensin II antagonist for the detection of renin-dependent high blood pressure was studied in renal hypertensive rats and in normotensive and hypertensive subjects. Infusion was started at a rate of 0.01 µg/kg × min saralasin and the dose was increased ten-fold at 15 min intervals. A significant fall of diastolic blood pressure was observed at the dose of 0.1 µg/kg × min in renal hypertensive rats, in healthy subjects treated with diuretics, and in patients with renovascular hypertension (saralasin responders). Plasma concentrations of angiotensin I, angiotensin II and of saralasin as well as plasma renin activity were measured. At the lowest infusion rate of 0.01 µg/kg × min, saralasin plasma levels were 40-fold higher than plasma angiotensin II levels. The decrease in arterial blood pressure occurred at lower doses of saralasin than the increase of plasma renin due to inhibition of feedback on the renin secreting cells. It is concluded that if the saralasin test is performed by a stepwise increase of the infusion rate, potentially dangerous complications such as hypoor hypertensive reactions can be avoided. The diagnostic reliability is improved by such a procedure since false positive and false negative responses may be prevented. The pressor effect of saralasin in non-renin dependent patients is an advantage since it causes a more marked difference of blood pressure change between saralasin responders and non-responders.
    Notes: Zusammenfassung Ein verbesserter Test zur Diagnose Renin-abhängiger Bluthochdruckformen mit dem Angiotensin II Rezeptor Antagonisten Saralasin wurde in hypertensiven Ratten, sowie in normotensiven und hypertensiven Patienten geprüft. Kumulative intravenöse Dosen, beginnend mit 0,01 µg/kg × min Saralasin wurde alle 15 Minuten um das zehnfache gesteigert. Ein signifikanter Blutdruckabfall bei der Dosis von 0,1 µg/kg × min wurde bei Ratten mit renaler Hypertonie, bei Patienten mit renaler Hypertonie und bei Patienten nach Diuretika-Vorbehandlung gefunden. Plasmaspiegel von Angiotensin I, Angiotensin II, Plasma Renin Aktivität und Saralasin wurden gemessen. Bei der niedrigsten Infusionsrate von 0,01 µg/kg × min waren die Saralasin-Konzentrationen im Plasma 40fach höher als die Plasma Angiotensin II-Konzentrationen. Der Blutdruckabfall erfolgte bei niedrigeren Dosen von Saralasin als der Anstieg von Plasma-Renin als Folge einer Hemmung des feedbacks der Reninsekretion. Die Ergebnisse zeigen, daß Komplikationen wie schwerwiegende Blutdruckanstiege und -abfälle bei schrittweiser Erhöhung der Saralasin-Infusionsrate vermieden werden können; gleichzeitig wird die diagnostische Zuverlässigkeit des Tests erhöht. Der geringe Angiotensin-ähnliche, blutdrucksteigernde Effekt von Saralasin bei Patienten mit niedrigem Renin wird als Vorteil ausgenutzt und erhöht den Unterschied der Blutdruckantwort bei Patienten mit hohem Plasma-Renin und Blutdruckabfall nach Saralasin-Infusion.
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