Salgado H C, Skelton M M, Salgado M C, Cowley A W
Department of Physiology, School of Medicine, Ribeirão Preto, SP, Brazil.
Hypertension. 1994 Jan;23(1 Suppl):I78-81. doi: 10.1161/01.hyp.23.1_suppl.i78.
We investigated the role of vasopressin, angiotensin II, and catecholamines in the onset of acute (45-minute) aortic coarctation hypertension in conscious rats. Partial aortic constriction was performed by means of a pneumatic cuff placed around the abdominal aorta above the renal arteries for 15 or 45 minutes. A sham-operated group was used as control. Mean carotid pressure before aortic constriction did not differ between rat groups. Aortic constriction produced a similar increase of mean carotid pressure during 15 minutes (36 +/- 3 to 37 +/- 3 mm Hg above basal levels) and 45 minutes (37 +/- 2 to 39 +/- 3 mm Hg). Plasma vasopressin concentration after 15 minutes of coarctation (4.4 +/- 0.5 pg/mL) did not differ from that observed in control rats (3.0 +/- 0.8 pg/mL), whereas after 45 minutes, it was significantly higher (14.3 +/- 3.3 pg/mL). Plasma renin activity increased significantly after coarctation (21.7 +/- 4.1 and 29.9 +/- 2.9 ng angiotensin I/mL per hour, at 15 and 45 minutes, respectively) when compared with control rats (3.9 +/- 0.5 ng angiotensin I/mL per hour). After coarctation, plasma norepinephrine concentration was consistently reduced, whereas plasma epinephrine concentration did not differ from control rats. In conclusion, these data provide evidence for an effective vasopressor role for vasopressin in the genesis of acute (45-minute) aortic coarctation hypertension in conscious rats. In addition, although the results confirm that the renin-angiotensin system participates earlier in the onset of coarctation hypertension, they rule out a significant vasopressor role for catecholamines in the early development of hypertension.
我们研究了血管加压素、血管紧张素II和儿茶酚胺在清醒大鼠急性（45分钟）主动脉缩窄性高血压发病中的作用。通过在肾动脉上方的腹主动脉周围放置气动袖带进行部分主动脉缩窄，持续15或45分钟。假手术组作为对照。主动脉缩窄前大鼠组的平均颈动脉压无差异。主动脉缩窄在15分钟（比基础水平高36±3至37±3 mmHg）和45分钟（比基础水平高37±2至39±3 mmHg）期间使平均颈动脉压产生类似程度的升高。缩窄15分钟后血浆血管加压素浓度（4.4±0.5 pg/mL）与对照大鼠（3.0±0.8 pg/mL）中观察到的浓度无差异，而45分钟后，其显著更高（14.3±3.3 pg/mL）。与对照大鼠（3.9±0.5 ng血管紧张素I/mL每小时）相比，缩窄后血浆肾素活性显著增加（15分钟和45分钟时分别为21.7±4.1和29.9±2.9 ng血管紧张素I/mL每小时）。缩窄后，血浆去甲肾上腺素浓度持续降低，而血浆肾上腺素浓度与对照大鼠无差异。总之，这些数据为血管加压素在清醒大鼠急性（45分钟）主动脉缩窄性高血压发病中发挥有效的升压作用提供了证据。此外, 虽然结果证实肾素 - 血管紧张素系统在缩窄性高血压发病中更早参与, 但排除了儿茶酚胺在高血压早期发展中发挥显著升压作用。
