Chalmers J, Minson J, Kapoor V, Cain M
J Hypertens Suppl. 1984 Dec;2(3):S37-9.
Lesions of the ventrolateral medulla coinciding with the A1 noradrenaline cell group, in either the rabbit or the rat, cause hypertension and bradycardia accompanied by 50-fold increases in plasma vasopressin and adrenaline and a two-to-four-fold increase in plasma noradrenaline. Following adrenalectomy in normal rats, the A1 hypertension and bradycardia were unchanged. In Brattleboro rats with diabetes insipidus, A1 hypertension was not altered but the bradycardia was reduced by 40%. In Brattleboro rats subjected to adrenalectomy, the hypertension was reduced by 50%. In normal rats, chemical sympathectomy with intravenous 6-hydroxydopamine (6OHDA) reduced the hypertension by about 50%, and when combined with adrenalectomy it abolished the hypertension altogether. In Brattleboro rats, 6OHDA reduced the hypertension after A1 lesions by about 40%. We suggest that A1 hypertension is predominantly mediated through increased activity of sympathetic vasoconstrictor nerves, and that circulating adrenaline and vasopressin only make a minor contribution to the increase in pressure.
在兔子或大鼠中，与A1去甲肾上腺素细胞群重合的延髓腹外侧病变会导致高血压和心动过缓，同时血浆血管加压素和肾上腺素增加50倍，血浆去甲肾上腺素增加2至4倍。正常大鼠肾上腺切除术后，A1高血压和心动过缓没有变化。在患有尿崩症的布拉特洛维大鼠中，A1高血压没有改变，但心动过缓减少了40%。对布拉特洛维大鼠进行肾上腺切除术后，高血压降低了50%。在正常大鼠中，静脉注射6-羟基多巴胺（6OHDA）进行化学交感神经切除术可使高血压降低约50%，与肾上腺切除术联合使用时，可完全消除高血压。在布拉特洛维大鼠中，6OHDA可使A1病变后的高血压降低约40%。我们认为，A1高血压主要是通过交感缩血管神经活动增加介导的，循环中的肾上腺素和血管加压素对血压升高的贡献较小。
