Young J B, Landsberg L
J Clin Invest. 1979 Jul;64(1):109-16. doi: 10.1172/JCI109429.
The pattern of urinary catecholamine excretion in fasting differs in pregnant and nonpregnant rats, which suggests that the sympathoadrenal response to fasting is altered by pregnancy. In fasting nonpregnant animals, urinary norepinephrine (NE) excretion decreases and epinephrine (E) excretion remains unchanged, whereas the excretion of both catecholamines rises significantly with refeeding. In contrast, fasting third-trimester pregnant rats exhibit a 420% increase in urinary E and a 345% increase in urinary NE, elevations which fall with refeeding. Specific evaluation of sympathoadrenal activity in fasting pregnant rats reveals stimulation of the adrenal medulla and suppression of sympathetic nerves. In fasting third-trimester rats the adrenal content of E is 37% lower in innervated adrenals as compared with contralateral denervated glands, which indicates the presence of neurally-mediated adrenal medullary activation. Adrenalectomy completely abolishes the fasting-induced rise in urinary E and NE in pregnant rats. Studies with 2-deoxy-D-glucose suggest that stimulation of the adrenal medulla results from hypoglycemia, which is present after 3 d of fasting in pregnant rats (plasma glucose 36.7 mg/dl). Sympathetic nervous system activity, as measured by [(3)H]NE turnover in the heart, decreases in fasting pregnant rats despite hypoglycemia, a response similar to that seen in fasting nonpregnant animals where plasma glucose is maintained above 50 mg/dl. The calculated NE turnover rate is 44% lower in 2-d fasted pregnant rats than in fed pregnant animals (17.6 +/- 1.3 vs. 31.3 +/- 1.8 ng NE/heart per h, respectively). Thus adrenal medullary and sympathetic nervous system responses in fasting pregnant rats appear to be dissociated, which suggests that diet-induced changes in sympathetic activity and stimulation of the adrenal medulla by hypoglycemia may be independently regulated.
禁食状态下,怀孕大鼠和未怀孕大鼠的尿儿茶酚胺排泄模式有所不同,这表明怀孕会改变交感肾上腺系统对禁食的反应。在禁食的未怀孕动物中,尿去甲肾上腺素(NE)排泄减少,肾上腺素(E)排泄保持不变,而再次进食时两种儿茶酚胺的排泄均显著增加。相比之下,禁食的孕晚期大鼠尿E增加420%,尿NE增加345%,再次进食后这些升高值下降。对禁食怀孕大鼠交感肾上腺活动的具体评估显示,肾上腺髓质受到刺激,交感神经受到抑制。在禁食的孕晚期大鼠中,与对侧去神经支配的腺体相比,有神经支配的肾上腺中E含量低37%,这表明存在神经介导的肾上腺髓质激活。肾上腺切除术完全消除了怀孕大鼠禁食诱导的尿E和NE升高。用2-脱氧-D-葡萄糖进行的研究表明,肾上腺髓质的刺激源于低血糖,怀孕大鼠禁食3天后会出现低血糖(血浆葡萄糖36.7mg/dl)。尽管存在低血糖,但通过心脏中[³H]NE周转率测量的交感神经系统活动在禁食的怀孕大鼠中下降,这一反应与禁食的未怀孕动物相似,在未怀孕动物中血浆葡萄糖维持在50mg/dl以上。禁食2天的怀孕大鼠计算出 的NE周转率比喂食的怀孕动物低44%(分别为17.6±1.3与31.3±1.8ng NE/心脏每小时)。因此,禁食怀孕大鼠的肾上腺髓质和交感神经系统反应似乎是分离的,这表明饮食诱导的交感活动变化和低血糖对肾上腺髓质的刺激可能是独立调节的。