Inhibition of Splenic Natural Killer Cell Activity During Rat

• Main Authors: Pan, Suei-ping, 潘燧萍
• Other Authors: Lin Mao-Tsun
• Format: Others
• Language: zh-TW
• Online Access: http://ndltd.ncl.edu.tw/handle/97411164257023761017

碩士 === 國立成功大學 === 生理學研究所 === 85 === Nitric oxide (NO) synthesized in the central nervous system (CNS) as well as in vascular endothelial cells. The role played by NO in central control of cardiovascular function are not well understood. Evidence has accumulated to implicate that the organum vasculosum laminae terminalis (OVLT; which is a non BBB protection region that contains NO synthase and is found to be innervated by monoaminegic nerve fibers.) may be involved in blood pressure regulation. In the present study, experiments were carried out to explore the possible role played by NO or catecholamine (CA) pathways in rat OVLT in regulation of blood pressure.First, intra-lateralventricular (lv) administration of NG-nitro-L-arginine methyl ester (L-NAME, a NO synthase inhibitor) produced an increase in arterial pressure but a decrease in OVLT NO release (detected by porphyrin/nafion coated carbon fiber electrodes), while lv or iv administration hydroxylamine (a NO donor) produced the opposite effects. Furthermore, direct administration of L-NAME into the OVLT increased arterial pressure. On the other hand, intra-OVLT injection of NO donors including hydroxylamine, S-nitro-N- acetylpenicillamine (SNAP), sodium nitroprusside (SNP) and sodium azide (NaN3) decreased arterial pressure. The depressor effect of intra-OVLT hydroxylamine was not inhibited by pretreatment with an intra-OVLT dose of methylene blue (MB, a guanylate cyclase inhibitor). Intra-OVLT injection of neither MB nor 8-Br-cGMP (a cGMP analogue) produced MAP changes. The increased arterial pressure elicited by intra-OVLT injection of L-NAME or the decreased arterial pressure produced by intra-OVLT injection of hydroxylamine was attenuated by spinal cord transection at C7. Furthermore, lv administration of L-NAME increased both the arterial pressure and OVLT CA release (deteted by carbon fiber electrodes), while lv administration of hydroxylamine, or SNP produced the opposite effects. Pretreatment of OVLT with 6-hydroxyldopamine (CA neurotoxin) attenuated the arterial pressure responses to intra-OVLT injection of L-NAME or hydroxylamine. Intra-OVLT injection of amphetamine (a CA releaser) also increased the arterial pressure. Pretreatment of OVLT with SCH23390 (a D1 receptor antagonist), sulpiride (a D2 receptor antagonist), or haloperidol (a nonselective D2,3 receptor antagonist) antagonized the pressor effect of Intra-OVLT injection of L- NAME. Intra-OVLT injection of SCH23390 (a D1 receptor antagonist), haloperidol (a nonselective D2,3 receptor antagonist), NPA (a D2 receptor agonist), clonidine (a (2 receptor agonist) or isoproterenol (a nonselective ( receptor agonist) decreased arterial pressure, while SKF38393 (a D1 receptor agonist), apomorphine (a nonselective D2,3 receptor agonist), sulpiride (a D2 receptor antagonist), phenylephrine (a (1 receptor agonist), yohimbine (a (2 receptor antagonist), phentolamine (a ( receptor antagonist), atenolol (a (1 receptor antagonist), or Propranolol (a ( receptor antagonist) produced the opposite effects. The data indicate that the NO-CA links in the OVLT of rat brain are involved in arterial pressure regulation. In the OVLT of rat brain, activation of NO synthase may inhibit CA release which lead to depressor effects, while inhibition of NO synthase may enhance CA release which result in pressor effects.