Chang P C, Kriek E, van Brummelen P
Department of Nephrology, University Hospital Leiden, The Netherlands.
J Hypertens. 1994 Feb;12(2):179-90.
To assess the contribution of the sympathetic nervous system to the hypertension in patients with longstanding essential hypertension.
Overall sympathetic function, presynaptic adrenoceptors and neuronal re-uptake were examined after withdrawal of medication for at least 3 weeks in eight patients with longstanding essential hypertension and in eight carefully matched normotensive control subjects.
Minimal forearm vascular resistance after 10 min ischaemia was used as a measure of structural vascular changes. Overall sympathetic tone was assessed using tilt testing and pressor dose infusion of noradrenaline. The presence and function of presynaptic adrenoceptors and the neuronal re-uptake of noradrenaline were evaluated in the forearm using tracer noradrenaline kinetics with measurement of forearm noradrenaline plasma appearance rate and noradrenaline plasma spillover. Intra-arterial infusions of tritiated noradrenaline, the endogenous alpha- and beta-adrenoceptor agonist adrenaline, the alpha-adrenoceptor blocker phentolamine, the non-adrenergic vasodilator sodium nitroprusside and the neuronal re-uptake inhibitor desipramine were given in the forearm.
We found that the hypertensives had higher minimal forearm vascular resistance, indicating structural vascular changes; decreased overall sympathetic activity, indicated by a lower basal whole-body noradrenaline production rate; enhanced vasopressor sensitivity for exogenously administered noradrenaline with decreased arterial baroreflex sensitivity; indications of decreased forearm neuronal re-uptake; evidence consistent with the presence of presynaptic, release-facilitating beta-adrenoceptors in the forearm, apparently not functionally different between the two groups; and undecisive evidence for the presence of functional presynaptic alpha-adrenoceptors in the forearm.
In patients with longstanding essential hypertension we found decreased overall sympathetic activity, with indications of decreased forearm neuronal re-uptake, which might have a compensatory role. We found indications of structural vascular changes and diminished baroreflex sensitivity in the hypertensives, which contribute to the hypertension. However, peripheral presynaptic, release-facilitating beta-adrenoceptors seem to be present, which are functionally not clearly different between the two groups. Observations on peripheral presynaptic alpha-adrenoceptors were inconclusive.
评估交感神经系统在长期原发性高血压患者高血压发病中的作用。
对8例长期原发性高血压患者和8例精心匹配的血压正常对照者在停药至少3周后检测其整体交感神经功能、突触前肾上腺素能受体和神经元再摄取情况。
以10分钟缺血后前臂最小血管阻力作为血管结构改变的指标。采用倾斜试验和去甲肾上腺素升压剂量输注评估整体交感神经张力。在前臂使用示踪去甲肾上腺素动力学方法，通过测量前臂去甲肾上腺素血浆出现率和去甲肾上腺素血浆溢出量，评估突触前肾上腺素能受体的存在及功能以及去甲肾上腺素的神经元再摄取情况。在前臂进行动脉内输注氚标记去甲肾上腺素、内源性α和β肾上腺素能受体激动剂肾上腺素、α肾上腺素能受体阻滞剂酚妥拉明、非肾上腺素能血管扩张剂硝普钠以及神经元再摄取抑制剂地昔帕明。
我们发现高血压患者前臂最小血管阻力较高，提示存在血管结构改变；整体交感神经活动降低，表现为基础全身去甲肾上腺素生成率较低；对外源性给予的去甲肾上腺素升压敏感性增强，动脉压力反射敏感性降低；前臂神经元再摄取减少的迹象；有证据表明前臂存在促进释放的突触前β肾上腺素能受体，两组之间在功能上无明显差异；关于前臂功能性突触前α肾上腺素能受体的存在证据不明确。
在长期原发性高血压患者中，我们发现整体交感神经活动降低，伴有前臂神经元再摄取减少的迹象，这可能具有代偿作用。我们发现高血压患者存在血管结构改变和压力反射敏感性降低的迹象，这有助于高血压的发生。然而，外周似乎存在促进释放的突触前β肾上腺素能受体，两组之间在功能上并无明显差异。关于外周突触前α肾上腺素能受体的观察结果尚无定论。
