Jablonskis L T, Howe P R
Division of Human Nutrition, Commonwealth Scientific and Industrial Research Organisation, Adelaide, South Australia.
J Hypertens. 1995 Mar;13(3):319-25.
To examine the relationship between plasma adrenaline and hypertension.
Plasma adrenaline responses to chronic manipulations of blood pressure were tested in normotensive and in hypertensive rats.
Hypertension was induced in normotensive Wistar-Kyoto (WKY) rats by administration of the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME), and blood pressure was lowered in stroke-prone spontaneously hypertensive rats (SHRSP) by administering hydralazine. Plasma catecholamine responses were monitored using blood samples from conscious unrestrained rats under resting conditions.
Twenty-four hours after starting L-NAME treatment, mean arterial pressure was 22 mmHg higher than in control WKY rats. Heart rate and plasma noradrenaline were reflexly reduced, but plasma adrenaline was unaffected. After 4 weeks of L-NAME treatment mean arterial pressure was 48 mmHg higher than in untreated rats. At this stage heart rate had returned to normal, but plasma noradrenaline was 33% higher and plasma adrenaline was 117% higher than in untreated rats. The elevation of plasma adrenaline was confirmed in a study of longer duration, in which plasma adrenaline had doubled after 10 weeks of L-NAME treatment. Conversely, 24 h after hydralazine treatment in SHRSP, mean arterial pressure was reduced by 49 mmHg and there was a reflex elevation of plasma adrenaline, noradrenaline and heart rate. However, after 19 days of blood pressure reduction with hydralazine, plasma noradrenaline and heart rate had returned to normal, but plasma adrenaline had fallen to 30% below normal. Most of the change in mean arterial pressure observed with either chronic L-NAME or hydralazine could be attributed to modulation of neurally mediated vasoconstriction, estimated from mean arterial pressure responses to acute autonomic blockade.
Selective changes in plasma adrenaline levels were induced by chronic experimental manipulations of blood pressure. This implies that the high plasma adrenaline level observed in spontaneously hypertensive rats might be a consequence rather than a cause of their hypertension.
研究血浆肾上腺素与高血压之间的关系。
在正常血压和高血压大鼠中测试血浆肾上腺素对血压长期调控的反应。
通过给予一氧化氮合酶抑制剂NG-硝基-L-精氨酸甲酯（L-NAME）诱导正常血压的Wistar-Kyoto（WKY）大鼠患高血压，并通过给予肼屈嗪降低易患中风的自发性高血压大鼠（SHRSP）的血压。在静息状态下，使用清醒自由活动大鼠的血样监测血浆儿茶酚胺反应。
开始L-NAME治疗24小时后，平均动脉压比对照WKY大鼠高22 mmHg。心率和血浆去甲肾上腺素反射性降低，但血浆肾上腺素未受影响。L-NAME治疗4周后，平均动脉压比未治疗大鼠高48 mmHg。此时心率已恢复正常，但血浆去甲肾上腺素比未治疗大鼠高33%，血浆肾上腺素比未治疗大鼠高117%。在一项持续时间更长的研究中证实了血浆肾上腺素的升高，其中L-NAME治疗10周后血浆肾上腺素增加了一倍。相反，在SHRSP中给予肼屈嗪治疗24小时后，平均动脉压降低了49 mmHg，血浆肾上腺素、去甲肾上腺素和心率反射性升高。然而，用肼屈嗪降低血压19天后，血浆去甲肾上腺素和心率已恢复正常，但血浆肾上腺素已降至比正常水平低30%。从急性自主神经阻滞的平均动脉压反应估计，慢性L-NAME或肼屈嗪引起的平均动脉压变化大部分可归因于神经介导的血管收缩的调节。
通过长期实验性血压调控可诱导血浆肾上腺素水平的选择性变化。这意味着在自发性高血压大鼠中观察到的高血浆肾上腺素水平可能是其高血压的结果而非原因。
