The Changes Of Neuronal Nitric Oxide Synthase And Insulin-like Growth Factor â…¡ Immunopositive Neurons And Ultrastructure Of Brain In SHR

Objective: This thesis was to discuss the effects of neuronal nitric oxide synthase (nNOS) and insulin-like growth factor-II (IGF-II) in the occurrence and development of hypertension by observing the changes of nitric oxide (NO) and IGF- II immunopositive neurons in the brain of spontaneous hypertension rats (SHR). Methods: 30 SHRs and Wistar-Koyto rats (WKYs) were separately used and sacrificed at the age of 3-, 6-, 12-months in order to observe the changes of nNOS and IGF- II immunopositive neurons after staining with ABC immunocytochemical assay and the changes of ultrastructure in cerebral cortex with the technique of transmission electron microscopic of each groups.Results: (1) Changes of the blood pressure: The blood pressure of 3-, 6-, and 12-month-old WKY was permanent, while the blood pressure of 3-, 6-, and 12-month-old SHR became higher and higher, which were obviously higher than those of the WKY. (2) Changes of the nNOS immunopositive neurons: The nNOS immunopositive neurons were changeless in each period, while the nNOS immunopositive neurons decreased with the ascending of blood pressure. The number of the nNOS immunopositive neurons in the central amygdaloid nucleus, accumbens nucleus, caudate putamen and the sensorimotor cortex decreases gradually. (3) Changes of the IGF-II immunopositive neurons: The nNOS immunopositive neurons were changeless in each period, while the IGF-II immunopositive neurons increase with the ascending of blood pressure. The number of the IGF-II immunopositive neurons in the cortex and caudate putamen increases gradually. (4) Changes of the ultrastructure: The neurons in the cortex of SHR with the ascending of blood pressure, appeared karyopyknosis, mitochondria swollen, crista lost, the membranes of pre-synaptic and post-synaptic were not clear and the synaptic space was disappeared. Conclusions: (1) The nNOS immunopositive neurons in central amygdaloid nucleus, accumbens nucleus, caudate putamen and the sensorimotor cortex of the SHR decreased in 3-, 6-, and 12-month. The diminution of NO especially in 12 months related to the imbalance of contraction and relaxation of the blood vessel, whichmaybe relate to the occurrence and development of hypertension. (2) The nNOS immunopositive neurons in central amygdaloid nucleus and accumbens nucleus of the SHR decreased. These led to the reduction of LTP, which was one of a possible reason of the decline in memory. (3) The nNOS immunopositive neurons in accumbens nucleus and the sensorimotor cortex of the SHR decreased. These maybe result from hypalgesia in hypertension through midbrain-limbic analgesia circuit. (4) By observation of ultrastructure, there were degeneration and necrosis occurred in the neurons of the cortex of SHR with the ascending of blood pressure. These maybe related to the structure of the brain in SHR was destroyed in different level. (5) The IGF-II immunopositive neurons in the cortex, caudate putamen increases with the ascending of blood pressure. The changes maybe have a protective action on the brain damage of hypertension.