Jest P, Pedersen K E, Klitgaard N A, Arentoft A, Nielsen J R
Department of Clinical Chemistry, Odense University Hospital, Denmark.
Scand J Clin Lab Invest. 1987 Dec;47(8):813-8.
Lymphocyte sodium content and sodium efflux were studied in 9 healthy normotensive males without history of essential hypertension before, during and after 5 weeks of severe sodium depletion. Sodium depletion caused a significant increase in sodium content and a slight but non-significant decrease in potassium content. Total and ouabain-sensitive sodium efflux rate constants decreased significantly during sodium depletion, while absolute sodium efflux, derived from cellular sodium concentration and the corresponding sodium efflux rate constants, remained unchanged. A significant reduction in arterial mean and diastolic blood pressure, measured by ambulatory as well as by home readings, was observed during salt restriction. Prolonged severe sodium depletion of normotensive subjects leads to changes in lymphocytic sodium homeostasis, probably due to a primary inhibition of the sodium pump and a secondary intralymphocytic sodium accumulation. The mechanism underlying these changes remains unclarified.
对9名无原发性高血压病史的健康血压正常男性,在严重钠耗竭前、期间和5周后,研究了淋巴细胞钠含量和钠流出情况。钠耗竭导致钠含量显著增加,钾含量轻微但不显著降低。在钠耗竭期间,总钠流出率常数和哇巴因敏感的钠流出率常数显著降低,而由细胞钠浓度和相应的钠流出率常数得出的绝对钠流出量保持不变。在限盐期间,通过动态血压监测和家庭血压测量均观察到动脉平均血压和舒张压显著降低。血压正常受试者长期严重钠耗竭会导致淋巴细胞钠稳态发生变化,这可能是由于钠泵的原发性抑制和淋巴细胞内继发性钠蓄积所致。这些变化的潜在机制尚不清楚。