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1 Research Equipment Center and 2 Department of Pharmacology, Kagawa Medical University, Kagawa 761-0793, Japan
The effect of
inhibition of nitric oxide (NO) synthesis on the responses of blood
pressure (BP), heart rate (HR), and renal sympathetic nerve activity
(RSNA) during hemorrhaging was examined with the use of an NO synthase
inhibitor,
NG-nitro-L-arginine
methyl ester (L-NAME), in
conscious rats. In the 0.9% saline group, hemorrhage (10 ml/kg body
wt) did not alter BP but significantly increased HR and RSNA by 88 ± 12 beats/min and 67 ± 12%, respectively. Intravenous
infusion of L-NAME (50 µg · kg
1 · min1)
significantly attenuated these tachycardic and sympathoexcitatory responses to hemorrhage (14 ± 7 beats/min and 26 ± 12%, respectively). Pretreatment of
L-arginine (87 mg/kg) recovered
the attenuation of HR and RSNA responses induced by
L-NAME (92 ± 6 beats/min and 64 ± 10%, respectively).
L-NAME by itself did not alter
the baroreceptor reflex control of HR and RSNA. Hemorrhage increased
the plasma vasopressin concentration, and its increment in the
L-NAME-treated group was
significantly higher than that in the 0.9% saline group. Pretreatment
with the vascular arginine vasopressin
V1-receptor antagonist OPC-21268
(5 mg/kg) recovered the attenuation of RSNA response induced by
L-NAME (54 ± 7%). These
results indicate that NO modulated HR and RSNA responses to hemorrhage
but did not directly affect the baroreceptor reflex arch. It can be
assumed that NO modulated the baroreflex function by altering the
secretion of vasopressin induced by hemorrhage.
heart rate; vasopressin
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