Badder E M, Duarte B, Seaton J F, Hamaji M, Harrison T S
Endocrinology. 1985 Nov;117(5):1920-9. doi: 10.1210/endo-117-5-1920.
Acute nephrectomy seriously impairs hypovolemic adrenal epinephrine (E) release in the anesthetized dog. That systemically delivered angiotensin II totally restores E release to acutely anephric dogs is equally clear, but the dose-response relationship of this angiotensin II effect is not known. Adrenal secretion rates and arterial plasma E, norepinephrine (NE), and dopamine levels were studied in nine groups of mongrel dogs (n = 5 in each group) under pentobarbital anesthesia: 1) resting animals; 2) hemorrhage (25 ml/kg); 3) hemorrhage after acute nephrectomy; 4-7) hemorrhage, acute nephrectomy, plus iv angiotensin II at a) 0.01 ng/kg X min, b) 0.10 ng/kg X min, c) 1.00 ng/kg X min, or d) 10.00 ng/kg X min; 8) no hemorrhage, acute nephrectomy, angiotensin II (10.00 ng/kg X min); and 9) hemorrhage, kidneys intact, iv angiotensin II (10.00 ng/kg X min). Arterial and adrenal blood were sampled during a baseline prehemorrhage period and 15, 30, 60, and 90 min after hemorrhage. We confirm blunting of reflex E release by acute nephrectomy in the anesthetized dog and show that angiotensin II restores E (P less than 0.01), NE (P less than 0.01), and dopamine (P less than 0.01) release in acutely anephric dogs. Aortic plasma E and NE were also restored to normal by angiotensin II (P less than 0.01 for each). Dogs with intact kidneys show a blunted hemorrhage response of arterial plasma E (P less than 0.01), NE (P less than 0.01), and DM (P less than 0.05) to our largest angiotensin II infusion rate (10 ng/kg X min). The study demonstrates that in acutely anephric conditions, angiotensin II support of reflex catecholamine release is sensitively dose dependent to physiological infusion rates of systemic angiotensin II and suggests further that this angiotensin II effect is restrained by the kidneys.
急性肾切除会严重损害麻醉犬低血容量时肾上腺肾上腺素（E）的释放。全身给予血管紧张素II能使急性无肾犬的E释放完全恢复，这一点同样明确，但这种血管紧张素II效应的剂量反应关系尚不清楚。在戊巴比妥麻醉下，对九组杂种犬（每组n = 5）的肾上腺分泌率以及动脉血浆E、去甲肾上腺素（NE）和多巴胺水平进行了研究：1）静息动物；2）出血（25 ml/kg）；3）急性肾切除后出血；4 - 7）出血、急性肾切除，加静脉注射血管紧张素II，剂量分别为a）0.01 ng/kg·min、b）0.10 ng/kg·min、c）1.00 ng/kg·min或d）10.00 ng/kg·min；8）无出血、急性肾切除、血管紧张素II（10.00 ng/kg·min）；9）出血、肾脏完整、静脉注射血管紧张素II（10.00 ng/kg·min）。在出血前的基线期以及出血后15、30、60和90分钟采集动脉血和肾上腺血样本。我们证实了急性肾切除会使麻醉犬反射性E释放减弱，并表明血管紧张素II能使急性无肾犬的E（P < 0.01）、NE（P < 0.01）和多巴胺（P < 0.01）释放恢复。血管紧张素II也使主动脉血浆E和NE恢复正常（每项P < 0.01）。肾脏完整的犬对我们最大血管紧张素II输注速率（10 ng/kg·min）时动脉血浆E（P < 0.01）、NE（P < 0.01）和多巴胺（P < 0.05）的出血反应减弱。该研究表明，在急性无肾情况下，血管紧张素II对反射性儿茶酚胺释放的支持对全身血管紧张素II的生理输注速率敏感地呈剂量依赖性，并且进一步表明这种血管紧张素II效应受到肾脏的抑制。
