Tobian L
Horm Res. 1979;11(6):277-91. doi: 10.1159/000179066.
Dahl 'S' rats become hypertensive when fed a high NaCl diet but remain normotensive on a low NaCl diet. Dahl 'R' rats are normotensive on either diet. For a given perfusion pressure, isolated 'S' kidneys excrete 50% less Na than 'R' kidneys. Therefore, we searched for a Na-retaining hormone in 'S' rats. Kidneys were isolated without ischemia from normal rats and were continuously perfused at 125 mm Hg with blood from Dahl 'S' and 'R' rats, all on low NaCl diets. Kidneys and adrenals had been extirpated from the perfusing rats. During 15 min of perfusion, the isolated 'normal' kidneys excreted a mean of 164 micronEq of Na/min/100 g during 26 perfusion experiments with blood from 'R' rats. The 'normal' kidneys excreted a mean of 84 micronEq Na during 24 perfusions with blood from 'S' rats. Thus, the normal kidneys excreted half as much Na when perfused with 'S' blood compared with 'R' blood (p less than 0.02). Seemingly, a Na-retaining humoral agent is present in the blood of 'S' rats on a low Na diet in the absence of renal and adrenal tissue. Moreover, in these normal kidneys, perfusion with 'S' blood induced a 16% higher renal vascular resistance than perfusion with 'R' blood (p less than 0.01), indicating vasoconstricting agents in 'S' blood. However, the Na-retaining humoral effect in 'S' blood could lead to Na retention by 'S' kidneys in vivo, which could partially account for the susceptibility of 'S' rats to NaCl hypertension. Hypertension in Dahl 'S' rats can be almost completely prevented by concomitant treatment with thiazide diuretics which act mainly on the kidney to facilitate Na excretion. This result is in agreement with the hypothesis that a shift in the pressure natriuresis curve, reducing Na excretion for a given arterial pressure, is partially responsible for the great sensitivity to NaCl hypertension in the 'S' rat. The Na-retaining hormone may contribute to this shift.
给予高盐饮食时，Dahl“S”大鼠会出现高血压，但给予低盐饮食时血压仍正常。Dahl“R”大鼠无论何种饮食血压均正常。在给定的灌注压力下，分离的“S”肾排出的钠比“R”肾少50%。因此，我们在“S”大鼠中寻找一种保钠激素。从正常大鼠中分离出肾脏，不进行缺血处理，然后用来自Dahl“S”和“R”大鼠的血液在125 mmHg下持续灌注，所有大鼠均给予低盐饮食。灌注大鼠的肾脏和肾上腺已被切除。在15分钟的灌注过程中，在26次用“R”大鼠血液进行的灌注实验中，分离的“正常”肾脏平均每分钟每100克排出164微当量的钠。在24次用“S”大鼠血液进行的灌注中，“正常”肾脏平均排出84微当量的钠。因此，与用“R”大鼠血液灌注相比，用“S”大鼠血液灌注时，正常肾脏排出的钠减少了一半（p<0.02）。显然，在没有肾和肾上腺组织的情况下，低钠饮食的“S”大鼠血液中存在一种保钠体液因子。此外，在这些正常肾脏中，用“S”大鼠血液灌注比用“R”大鼠血液灌注诱导的肾血管阻力高16%（p<0.01），表明“S”大鼠血液中存在血管收缩剂。然而，“S”大鼠血液中的保钠体液效应可能导致“S”肾在体内潴留钠，这可能部分解释了“S”大鼠对盐性高血压的易感性。噻嗪类利尿剂主要作用于肾脏以促进钠排泄，联合使用噻嗪类利尿剂几乎可以完全预防Dahl“S”大鼠的高血压。这一结果与以下假设一致，即压力-利钠曲线的偏移，在给定动脉压下减少钠排泄，部分导致了“S”大鼠对盐性高血压的高度敏感性。保钠激素可能促成了这种偏移。
