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Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka 812-82, Japan
We
examined the role of central nitric oxide (NO) in the baroreceptor
reflex in conscious rabbits. Intracerebroventricular infusion of 20 µmol of N 
-nitro-L-arginine
methyl ester (L-NAME) to block
central NO resulted in increases in arterial pressure, renal
sympathetic nerve activity (RSNA), and plasma catecholamine levels, and
the pressor response was suppressed by pretreatment with pentolinium (5 mg/kg iv). On the other hand, a subpressor dose of
intracerebroventricular L-NAME
(10 µmol/h) caused significant increases in baroreflex sensitivities
assessed by RSNA and heart rate compared with vehicle infusion
[maximum gain: 
18.2 ± 0.9 vs. 9.6 ± 0.9%/mmHg (P < 0.001) and
14.3 ± 2.3 vs. 5.7 ± 0.4 beats · min
1 · mmHg1
(P < 0.05), respectively].
Conversely, an intracerebroventricular infusion of
Et2N[N(O)NO]Na, an NO
donor (1 µmol/h) significantly attenuated the baroreflex
sensitivities. However, intracerebroventricular infusion of
N -nitro-D-arginine
methyl ester (10 µmol/h), an enantiomer of
L-NAME, failed to alter the
baroreflex sensitivities. These results suggest that
1) the pressor response induced by
inhibition of central NO synthesis is mainly mediated by the enhanced
sympathetic outflow and 2) central
NO attenuates the baroreflex control of RSNA and heart rate in
conscious rabbits.
catecholamines; central nervous system; renal sympathetic nerve activity; sympathetic nervous system
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