Renal Na+‐K+‐ATPase in Okamoto and Dahl Hypertensive Rats
Renal Na+‐K+‐ATPase in Okamoto and Dahl Hypertensive Rats
复制标题
冈本和达尔高血压大鼠的肾 Na+‐K+‐ATP 酶
作者：
C. Rodríguez;J. Cangiano;S. Opava
测定了两组8只自发性高血压大鼠（SHR）、两组8只达尔盐高血压大鼠（SS）及其对照（16只正常Wistar大鼠和16只耐盐大鼠）血浆肾素活性（PRA, ng Al/ml/hr）、血浆醛固酮（PA, ng%）和肾Na+- k +- atp酶（pm PO</mg protein/hr）。一组在正常（0.48%钠）饮食2周后进行测量，另一组在低钠（0.01%钠）饮食2周后进行测量。在正常钠饮食后，两组高血压大鼠的PRA和PA均低于对照组正常动物。SS组肾Na+-K+- atp酶低于对照组，SHR组与对照组无显著差异。在无钠饮食中，SHR表现出肾脏Na+-K+- atp酶升高，但PRA和PA保持低水平。相比之下，在相似的条件下，SS大鼠的PRA、PA和肾脏Na+-K+- atp酶升高，尽管程度低于sr大鼠。这些结果表明，在基础条件下和低盐饮食后，SHR大鼠的肾脏Na+-K+- atp酶活性与正常大鼠一样。然而，SHR的变化与PA无关。SS中PRA和PA的减少提示体积扩张性高血压。SHR不存在体积扩张，肾Na+- k +- atp酶不改变。SS组酶活性低于SHR组和对照组。这提示，容量扩张导致的某些因素可能是抑制肾Na+-K+- atp酶的原因。（高血压3（补充II）： II-86-II-91, 1981）
SUMMARY Plasma renin activity (PRA, ng Al/ml/hr), plasma aldosterone (PA, ng%) and renal Na+-K+- ATPase (pm PO</mg protein/hr) were measured in two groups of eight spontaneously hypertensive rats (SHR), two groups of eight Dahl salt hypertensive rats (SS), and their controls (16 normal Wistar and 16 saltresistant rats). Measurements were made in one group after 2 weeks on a normal (0.48% sodium) and in the other group after 2 weeks on a low (0.01% sodium) sodium diet. After a normal sodium diet, PRA and PA were lower in both groups of hypertensive rats than in control normotensive animals. Renal Na+-K+-ATPase was lower in SS than in controls: in SHR it was not different from control. On a sodium-free diet, SHR exhibited a rise in renal Na+-K+-ATPase but PRA and PA remained low. In contrast, under similar conditions PRA, PA, and renal Na+-K+-ATPase increased in SS rats, although to a lesser extent than in SR. These results suggest that under basal conditions and after low salt diet, renal Na+-K+-ATPtse activity in SHR behaves as it does in normal rats. However, the changes are independent of PA in SHR. The reduction in PRA and PA in SS suggests volume expansion hypertension. In SHR, volume expansion is not present, and renal Na+-K+- ATPase is not altered. Enzyme activity is lower in SS than in SHR and control. This suggests that some factor that results from volume expansion may be responsible for inhibition of renal Na+-K+-ATPase. (Hypertension 3 (suppl II): II-86-II-91, 1981)