Access Type

Open Access Dissertation

Date of Award


Degree Type


Degree Name




First Advisor

Joseph C. Dunbar, Ph.D.


Insulin and insulin-like growth factor 1 (IGF-l) share some structure homologies and exert similar metabolic as well as cardiovascular actions. Insulin and IGF-l have been demonstrated to decrease cardiovascular tone and increase blood flows in skeletal muscle. Insulin has also been showed to increase sympathetic nerve activity that may play a role in the regulation of cardiovascular dynamics. This study investigated the effects of insulin and IGF-l on cardiovascular parameters and sympathetic nerve activity and the correlation between them. We also evaluated the role of baroreflex, plasma glucose level and regional sympathectomy in those insulin and IGF-l induced responses. Normal wistar rats were anesthetized with chloralose/urethane. The femoral artery and vein were cannulated to monitor mean arterial pressure (MAP) and heart rate (HR) or for infusion or blood sampling. The lumbar sympathetic nerve or renal sympathetic nerve was isolated and placed on electrodes for nerve activity recording. Electromagnetic flow probes were placed around the iliac arteries for blood flow measurement. The systemic administration of insulin and IGF-l resulted in significant decrease in MAP. Insulin increased lumbar sympathetic nerve activity (LSNA) independent of the prevailing glucose concentration and baroreflex. It increased renal sympathetic nerve activity (RSNA) only under hypoglycemia condition. IGF-l decreased both LSNA and SNA, but this effect was modulated by glycemic status. Lumbar sympathectomy caused greater increase in skeletal muscle blood flow in response to both insulin and IGF-l when hypoglycemia occurred. But when hypoglycemia was prevented, GF-l induced increase in blood flow was suppressed in sympathetic denervated iliac artery. We concluded that insulin and IGF-l have both similar and distinct effects on cardiovascular system and sympathetic nervous system. They both may act directly on asculature to elicit vasodilation thus decrease MAP. Insulin can selectively increase sympathetic nerve activity, while IGF-l decreases sympathetic nerve activity. These processes are modulated by glycemic status. Baroreflex may be involved but is not responsible for them.