| Summary: | 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.
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