Fujii T, Inoue S, Nagai K, Nakagawa H
Third Department of Internal Medicine, Yokohama City University, Japan.
Horm Metab Res. 1989 Dec;21(12):643-5. doi: 10.1055/s-2007-1009309.
Previously we found that in rats, electrical stimulation of the suprachiasmatic nucleus (SCN) of the hypothalamus elicited hyperglycemia associated with hyperglucagonemia without immediate hyperinsulinemia. To clarify the mechanism of these responses, we examined the effects of blockers of the autonomic nervous system on these responses. Hexamethonium, a ganglion blocker, suppressed the hyperglycemic and hyperglucagonemic responses to electrical stimulation of the SCN. Both bunazosin, an alpha 1-adrenergic blocker, and yohimbin, an alpha 2-adrenergic blocker, increased the level of insulin before stimulation, but only the latter suppressed the hyperglycemic and hyperglucagonemic responses. Propranolol, a beta-adrenergic blocker, partially inhibited the responses. These findings suggest that alpha 2- and beta-adrenergic mechanisms are involved in the hyperglycemic and hyperglucagonemic responses to SCN stimulation.
此前我们发现，在大鼠中，电刺激下丘脑视交叉上核（SCN）会引发高血糖，并伴有高胰高血糖素血症，且无即时高胰岛素血症。为阐明这些反应的机制，我们研究了自主神经系统阻滞剂对这些反应的影响。神经节阻滞剂六甲铵可抑制对SCN电刺激的高血糖和高胰高血糖素反应。α1肾上腺素能阻滞剂布那唑嗪和α2肾上腺素能阻滞剂育亨宾在刺激前均能提高胰岛素水平，但只有后者能抑制高血糖和高胰高血糖素反应。β肾上腺素能阻滞剂普萘洛尔可部分抑制这些反应。这些发现表明，α2和β肾上腺素能机制参与了对SCN刺激的高血糖和高胰高血糖素反应。
