Golczynska A, Lenders J W, Goldstein D S
Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
Clin Pharmacol Ther. 1995 Jul;58(1):90-8. doi: 10.1016/0009-9236(95)90076-4.
To test whether glucocorticoids inhibit sympathetic nerve activity or norepinephrine release in humans, as has been suggested by results in laboratory animals.
This was a double-blind, placebo-controlled, randomized crossover study performed at the Clinical Center of the National Institutes of Health. Thirteen normal volunteers received 20 mg prednisone or placebo orally each morning for 1 week, followed by a washout period of 1 week and then by treatment with the other drug for 1 week. On the last day of each treatment week, blood samples were drawn for measurements of plasma levels of catecholamines and their metabolites, of cortisol, and of corticotropin at baseline and during reflexive sympathetic stimulation elicited by lower body negative pressure (-15 mm Hg). A 24-hour urine collection was obtained at the end of each week of treatment for measurement of urinary excretion of catechols. In eight subjects, directly recorded peroneal skeletal muscle sympathetic nerve activity was also measured after both treatments.
Prednisone significantly decreased sympathetic nerve activity by 23% +/- 6%, plasma norepinephrine levels by 27% +/- 6%, and plasma corticotropin levels by 77%. Blood pressure, heart rate, body weight, and urinary excretion of catechols and electrolytes were unaffected. Prednisone did not alter proportionate increments in sympathetic nerve activity or plasma norepinephrine levels during lower body negative pressure. Relationships between sympathetic nerve activity and plasma norepinephrine levels were unchanged.
Glucocorticoids decrease sympathoneural outflows in humans without affecting acute sympathoneural responses to decreased cardiac filling and probably without affecting presynaptic modulation of norepinephrine release.
如实验室动物实验结果所示，测试糖皮质激素是否会抑制人类的交感神经活动或去甲肾上腺素释放。
这是一项在美国国立卫生研究院临床中心进行的双盲、安慰剂对照、随机交叉研究。13名正常志愿者每天早晨口服20毫克泼尼松或安慰剂，持续1周，随后有1周的洗脱期，然后用另一种药物治疗1周。在每个治疗周的最后一天，采集血样以测量基线时以及下体负压（-15毫米汞柱）引起的反射性交感神经刺激期间血浆儿茶酚胺及其代谢产物、皮质醇和促肾上腺皮质激素的水平。在每个治疗周结束时收集24小时尿液，以测量儿茶酚的尿排泄量。在8名受试者中，还在两种治疗后测量了直接记录的腓骨骨骼肌交感神经活动。
泼尼松使交感神经活动显著降低23%±6%，血浆去甲肾上腺素水平降低27%±6%，血浆促肾上腺皮质激素水平降低77%。血压、心率、体重以及儿茶酚和电解质的尿排泄量均未受影响。泼尼松在下体负压期间未改变交感神经活动或血浆去甲肾上腺素水平的相应增加。交感神经活动与血浆去甲肾上腺素水平之间的关系未改变。
糖皮质激素可降低人类的交感神经输出，而不影响对心脏充盈减少的急性交感神经反应，并且可能不影响去甲肾上腺素释放的突触前调节。
