Kubo T, Amano H
Brain Res. 1986 Jan 15;363(1):183-7. doi: 10.1016/0006-8993(86)90676-1.
Bilateral electrolytic lesioning of the nucleus tractus solitarii elicited a pressor response in rats with spinal transection. This response was abolished by a vasopressin pressor antagonist and plasma vasopressin was increased during the response. This evidence suggests that the nucleus tractus solitarii is involved in inhibiting vasopressin release and that an impaired function would lead to an enhancement of vasopressin release, to the extent of eliciting a pressor response.
在脊髓横断的大鼠中，双侧孤束核电解损伤引发了升压反应。这种反应被一种血管升压素升压拮抗剂消除，且在反应过程中血浆血管升压素增加。这一证据表明，孤束核参与抑制血管升压素释放，其功能受损会导致血管升压素释放增强，甚至引发升压反应。
