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清醒肾血管性高血压兔应激时心脏和肾脏压力反射控制:利美尼定的作用

Cardiac and renal baroreflex control during stress in conscious renovascular hypertensive rabbits: effect of rilmenidine.

作者信息

Burke Sandra L, Head Goeffrey A

机构信息

Neuropharmacology Laboratory, Baker Heart Research Institute, Melbourne, Australia.

出版信息

J Hypertens. 2009 Jan;27(1):132-41. doi: 10.1097/hjh.0b013e328317a7a7.

DOI:10.1097/hjh.0b013e328317a7a7
PMID:19145779
Abstract

OBJECTIVE

We examined whether renal sympathetic nerve activity (RSNA) and heart rate (HR) baroreflexes in conscious rabbits were altered by exposure to a combination of stress and hypertension and determined how this was modified by acute and chronic treatment with the sympathoinhibitory agent rilmenidine.

METHODS

Rabbits were made hypertensive with a renal-artery clip and a renal nerve recording electrode was implanted 4-5 weeks later. After recovery, baroreflexes were measured before and during airjet stress and again after receiving rilmenidine (either acutely or by infusion for 3 weeks).

RESULTS

Renal clipping increased mean arterial pressure (MAP) and shifted baroreflex RSNA and HR curves rightward. The HR and RSNA upper plateaus were similar to those of normotensive animals but HR baroreflex sensitivity was reduced in the hypertensive group. Airjet stress lowered HR baroreflex sensitivity in sham but not in hypertensive rabbits. By contrast, stress increased the baroreflex-induced maximum RSNA in hypertensive animals but not in normotensive rabbits. MAP variability was greater in the hypertensive group but was unaffected by airjet stress. Acute and chronic rilmenidine lowered MAP to close to normotensive levels, markedly reduced MAP variability and RSNA but did not prevent the RSNA baroreflex facilitation produced by airjet stress.

CONCLUSION

Baroreflex control of HR was diminished by either hypertension or acute airjet stress but the effects were not additive. Although the baroreflex-induced RSNA maximum was increased by stress only in hypertensive animals, rilmenidine was effective in minimizing the reflex autonomic disturbances produced by hypertension and stress.

摘要

目的

我们研究了清醒家兔的肾交感神经活动(RSNA)和心率(HR)压力反射是否会因暴露于应激和高血压的联合作用而改变,并确定了交感神经抑制药利美尼定的急性和慢性治疗如何对其产生影响。

方法

通过肾动脉夹使家兔产生高血压,4至5周后植入肾神经记录电极。恢复后,在喷气应激前和应激期间测量压力反射,在给予利美尼定(急性给药或输注3周)后再次测量。

结果

肾动脉夹闭增加了平均动脉压(MAP),并使压力反射的RSNA和HR曲线向右移位。HR和RSNA的上限与正常血压动物相似,但高血压组的HR压力反射敏感性降低。喷气应激降低了假手术组家兔的HR压力反射敏感性,但对高血压家兔没有影响。相比之下,应激增加了高血压动物压力反射诱导的最大RSNA,但对正常血压家兔没有影响。高血压组的MAP变异性更大,但不受喷气应激的影响。急性和慢性利美尼定将MAP降至接近正常血压水平,显著降低了MAP变异性和RSNA,但并未阻止喷气应激产生的RSNA压力反射易化作用。

结论

高血压或急性喷气应激均可降低压力反射对HR的控制,但二者的影响并非相加性的。虽然仅在高血压动物中应激会增加压力反射诱导的RSNA最大值,但利美尼定可有效减轻高血压和应激产生的反射性自主神经紊乱。

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