Ernsberger P, Azar S, Azar P
Brain Res Bull. 1985 Dec;15(6):651-6. doi: 10.1016/0361-9230(85)90214-x.
Radiofrequency lesions were placed in the anteromedial hypothalamus in Dahl rats to investigate the role of this area in salt-induced hypertension. Lesions of the paraventricular and suprachiasmatic nuclei and intervening tissue (PVN-SCN lesions) prevented the rise in blood pressure (mmHg) in salt-sensitive (DS) rats fed a high-salt (8% NaCl) diet for 15 weeks (controls: 195 +/- 9, lesioned: 128 +/- 11, p less than 0.01). Similar lesions in salt-resistant (DR) rats did not alter long-term blood pressure (controls: 121 +/- 6 mmHg, lesioned: 131 +/- 5). Lesions sparing the PVN had no effect on blood pressure in DS rats, while lesions primarily confined to the PVN delayed the rise of blood pressure in DS fed a high salt diet. Round-the-clock determinations demonstrated that the blood pressure of DS rats with PVN-SCN lesions was reduced relative to controls at all times of the day throughout the study. No differences were observed between the angiotensin-induced drinking and plasma sodium concentrations of rats with PVN-SCN lesions and those of controls. Twenty-four hour mean heart rate was decreased by 10% in DS rats with PVN-SCN lesions. The anteromedial hypothalamus may participate in the initiation of Dahl hypertension.
在 Dahl 大鼠的下丘脑前内侧部位进行射频损伤，以研究该区域在盐诱导的高血压中所起的作用。对室旁核和视交叉上核以及其间组织进行损伤（PVN-SCN 损伤），可防止盐敏感（DS）大鼠在喂食高盐（8% NaCl）饮食 15 周后血压升高（mmHg）（对照组：195±9，损伤组：128±11，p＜0.01）。盐抵抗（DR）大鼠进行类似损伤并未改变其长期血压（对照组：121±6 mmHg，损伤组：131±5）。保留室旁核的损伤对 DS 大鼠血压无影响，而主要局限于室旁核的损伤则延缓了喂食高盐饮食的 DS 大鼠血压的升高。全天候测定表明，在整个研究过程中，具有 PVN-SCN 损伤的 DS 大鼠的血压在一天中的所有时间相对于对照组均有所降低。PVN-SCN 损伤大鼠与对照组在血管紧张素诱导的饮水和血浆钠浓度方面未观察到差异。具有 PVN-SCN 损伤的 DS 大鼠 24 小时平均心率降低了 10%。下丘脑前内侧可能参与了 Dahl 高血压的起始过程。
