We previously found that kidneys isolated from salt-restricted rats were refractory to atrial natriuretic peptide compared with kidneys from salt-loaded rats. Because the intrarenal tissue renin-angiotensin system may modulate renal responses to atrial natriuretic peptide, we examined the effect of dietary NaCl loading on the responses of isolated perfused kidneys from normal rats to atrial natriuretic peptide, before and after the addition of angiotensin II receptor antagonists or angiotensin I converting enzyme inhibitors to the perfusate. 2. Atrial natriuretic peptide increased the glomerular filtration rate and sodium excretion of kidneys from NaCl-loaded rats. The addition of angiotensin receptor antagonists or converting enzyme inhibitors partially reversed the increments in glomerular filtration rate but not the increments in sodium excretion, leading to an increased fractional sodium excretion. In the absence of atrial natriuretic peptide, these agents did not affect glomerular filtration or sodium excretion. Kidneys from NaCl-restricted rats did not respond to atrial natriuretic peptide or to the inhibitors and antagonists, either separately or in combination. 3. After NaCl loading, the intrarenal renin-angiotensin system may augment the glomerular response to atrial natriuretic peptide while simultaneously inhibiting the natriuretic response to atrial natriuretic peptide. However, activation of the intrarenal renin-angiotensin system is not responsible for the refractoriness of kidneys from salt-restricted rats to atrial natriuretic peptide.
摘要
我们之前发现，与盐负荷大鼠的肾脏相比，从限盐大鼠分离出的肾脏对心房利钠肽不敏感。由于肾内组织肾素 - 血管紧张素系统可能调节肾脏对心房利钠肽的反应，我们在向灌注液中添加血管紧张素 II 受体拮抗剂或血管紧张素 I 转换酶抑制剂之前和之后，研究了饮食中 NaCl 负荷对正常大鼠分离的灌注肾脏对心房利钠肽反应的影响。2. 心房利钠肽增加了盐负荷大鼠肾脏的肾小球滤过率和钠排泄。添加血管紧张素受体拮抗剂或转换酶抑制剂部分逆转了肾小球滤过率的增加，但没有逆转钠排泄的增加，导致钠排泄分数增加。在没有心房利钠肽的情况下，这些药物不影响肾小球滤过或钠排泄。限盐大鼠的肾脏对心房利钠肽或抑制剂及拮抗剂单独或联合使用均无反应。3. NaCl 负荷后，肾内肾素 - 血管紧张素系统可能增强肾小球对心房利钠肽的反应，同时抑制对心房利钠肽的利钠反应。然而，肾内肾素 - 血管紧张素系统的激活并非限盐大鼠肾脏对心房利钠肽不敏感的原因。
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