Modulation of Baroreflex Response by Prostaglandin I2 in the Nucleus Tractus Solitarii of the Rat

• Main Authors: Cheng-Yi Huang, 黃正義
• Other Authors: Jiin-Cherng Yen
• Format: Others
• Language: zh-TW
• Published: 2004
• Online Access: http://ndltd.ncl.edu.tw/handle/44966286844924232739

碩士 === 國立陽明大學 === 藥理學研究所 === 92 === Prostaglandin I2 (PGI2), derived from arachidonate metabolites, which exerts the potent ability in vasodilation and anti-platelet aggregation. During the past decades, numerous studies have suggested that PGI2 is produced mainly in the vascular endothelium. Further, recent evidence indicated that PGI2 could also be produced in central nervous system. Nucleus tractus solitarii (NTS), the primary terminal site of baroreceptor afferents, plays a principal role in the baroreceptor reflex (BRR) response. Besides, previous studies evidenced that cyclooxygenase (COX) and PGI2 receptor are located in NTS. However, the physiological role of PGI2 in NTS is still unclear. In the present study, immunhistochemical staining illustrates that the PGI2 synthase (PGIS) is abundant expressed in NTS, co-localized with neuronal nucleus protein (NeuN) and ionotropic glutamate receptors. Furthermore, bilateral microinjection with PGIS inhibitors in dorsal NTS enhanced the BRR response but suppressed response exhibits in ventral NTS. Bilateral microinjection of iloprost (a stable analogue of PGI2) significantly suppressed the BRR response in dorsal NTS. Inversely, microinjections of iloprost into ventral NTS enhanced the BRR response. On the other hand, the enhanced BRR response caused by iloprost was attenuated by co-microinjection with the non-selective nitric oxide synthase (NOS) inhibitor or neuronal nitric oxide synthase (nNOS) inhibitor in ventral NTS. The promotional effects of iloprost on the BRR response was completely abolished by microinjection of ipratropium (the peripheral muscarinic blocker), but showing no effects by microinjection of atenolol (the peripheral β-adrenoceptors blocker). These results together suggest that endogenous PGI2 in the dorsal NTS may play a suppressive role in BRR response, and iloprost may play a modulatory role in the BRR response via a central nitric oxide dependent vagal nerve mechanism.