Changes in renal angiotensin II receptors in spontaneously hypertensive rats by early treatment with the angiotensin-converting enzyme inhibitor captopril.
Changes in renal angiotensin II receptors in spontaneously hypertensive rats by early treatment with the angiotensin-converting enzyme inhibitor captopril.
复制标题
早期使用血管紧张素转换酶抑制剂卡托普利治疗自发性高血压大鼠肾血管紧张素 II 受体的变化。
DOI：
10.1161/01.hyp.23.6.819
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Berecek,KH
中科院分区：
文献类型：
--
作者：
Wu,JN;Edwards,D;Berecek,KH
我们测试的假设，在子宫内治疗血管紧张素转换酶抑制剂卡托普利可以改变亲和力，密度和/或亚型的血管紧张素II（Ang II）受体在自发性高血压大鼠（SHR）的肾脏。使用新生、7日龄和4月龄SHR和Wistar-Kyoto（WKY）大鼠。SHR和WKY大鼠饲养员用饮用水中的卡托普利（0.4 mg/mL，100 mg/kg/天）治疗，其幼崽保持在卡托普利治疗直至实验。对照组为未处理的、年龄匹配的SHR和WKY大鼠。使用放射性配体结合技术和对Ang II受体亚型1和2具有特异性的受体拮抗剂（氯沙坦，一种AT 1特异性拮抗剂，和CGP 42112 B，一种AT 2特异性拮抗剂）测定肾Ang II受体的密度、亲和力和亚型。新生大鼠和成年大鼠肾脏AT_1受体密度均高于AT_2受体密度。在所有组中，从出生到7日龄，肾脏中的AT 1受体密度增加约两倍。新生儿和7日龄SHR的肾脏血管紧张素II受体密度显着高于其他大鼠组，因为显着更大的密度的AT 1和AT 2受体。在4个月大时，卡托普利治疗组和对照组SHR肾脏中Ang II受体密度无显著差异。我们的数据表明，AT 1和AT 2受体在肾脏中的表达差异调节在发展过程中。新生儿和胎儿SHR肾组织中肾素-血管紧张素Ⅱ系统活性增强可能参与了高血压的发病机制。（250字处删节）
We tested the hypothesis that in utero treatment with the angiotensin-converting enzyme inhibitor captopril could change the affinity, density, and/or subtypes of angiotensin II (Ang II) receptors in the kidneys of spontaneously hypertensive rats (SHR). Newborn, 7-day-old, and 4-month-old SHR and Wistar-Kyoto (WKY) rats were used. SHR and WKY rat breeders were treated with captopril (0.4 mg/mL, 100 mg/kg per day) in drinking water, and their pups were maintained on captopril treatment until experimentation. Control groups were untreated, age-matched SHR and WKY rats. The density, affinity, and subtypes of renal Ang II receptors were determined using radioligand binding techniques and receptor antagonists specific for Ang II receptor subtypes 1 and 2 (losartan, an AT1-specific antagonist, and CGP 42112B, an AT2-specific antagonist). AT1 receptor density in kidneys was higher than AT2 receptor density in both neonatal and adult rats. AT1 receptor density in kidneys increased approximately twofold from birth to 7 days of age in all groups. Newborn and 7-day-old SHR showed significantly greater Ang II receptor densities in kidneys than other rat groups because of significantly greater densities of both AT1 and AT2 receptors. At 4 months of age, there were no significant differences in Ang II receptor densities in kidneys between captopril-treated and control SHR. Our data indicate that the expression of AT1 and AT2 receptors in kidneys is differentially regulated during development. Enhanced activity of the renal renin-Ang II system in newborn and probably fetal SHR may be involved in the pathogenesis of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)