大鼠正中视前核血管紧张素II型1受体的激活可诱导利尿和利钠反应

Yuan Gao, Lei Luo, Hong Liu
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引用次数: 0

摘要

目的探讨大鼠视前正中核(MnPO)血管紧张素II (AngII) 1型(AT1)受体激活对肾钠排泄的影响。方法麻醉后,大鼠经植入式插管注射到MnPO中。膀胱插管取尿样,火焰分光光度法测定尿钠浓度。用放射免疫法和钼磷铵法分别测定大鼠血清内源性地黄样因子(EDLF)水平和肾皮质组织Na+、K+- atp酶活性。结果尿量和钠排泄量在给药后60min达到峰值。这些反应伴随着血清EDLF的增加和肾皮质Na+, K+- atp酶活性的降低。AngII受体阻滞剂氯沙坦进入MnPO后可抑制MnPO对利尿和利钠的反应,以及血清EDLF升高和肾皮质Na+、K+- atp酶活性降低。结论大鼠MnPO中AT1受体的激活可诱导利尿和利钠反应。这些反应与EDLF的释放增加以及肾皮质组织中Na+,K+- atp酶活性的抑制有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Activation of angiotensin II type 1 receptors in the median preoptic nucleus induces a diuretic and natriuretic response in rats

Objective

To investigate the effect of activation of angiotensin II (AngII) type 1 (AT1) receptors in the median preoptic nucleus (MnPO) of rats on renal sodium excretion.

Methods

After anesthesia, the rats were injected into the MnPO via an implanted cannula. Urine samples were collected via a bladder cannula, and the urine sodium concentration was assayed with flame spectrophotometry. The serum level of endogenous digitalis-like factor (EDLF) and Na+, K+-ATPase activity in the renal cortex tissue were assayed respectively with a radioimmunoassay and with an ammonium molybdophosphate-based kit.

Results

Both the urinary volume and the sodium excretion peaked 60 min after AngII was administered into the MnPO. The responses were accompanied by an increase in serum EDLF and a decrease in Na+, K+-ATPase activity in the renal cortex. The responses of diuresis and natriuresis, as well as an increase in serum EDLF and a decrease in Na+, K+-ATPase activity in the renal cortex induced by MnPO adminstration with AngII were inhibited by pior treatment with the AngII receptor blocking agent losartan into the MnPO.

Conclusion

These results suggest that activation of AT1 receptors in the MnPO of rat induces diuretic and natriuretic responses. The responses are associated with an increase release of EDLF and with the inhibition of Na+,K+-ATPase activity in renal cortex tissue.

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