| Inhibition of
Beta-1 Receptor but not Vagotomy Can Abolish the
L-NAME Evoked Bradycardia in Anesthetized Rat
J.
VÁG, CS. HABLY1, J.
BARTHA1, P. MACKOWIAK1
Semmelweis
University, Department of Conservative Dentistry
and 1Department of
Physiology, Budapest, Hungary
Received June 11, 2001
Accepted October 11, 2001
Summary
We reported previously that the nitric
oxide synthesis inhibitor Nv-nitro-L-arginine
methyl ester (L-NAME) decreases cardiac output.
Several studies have shown that inhibition of
nitric oxide synthesis decreases the heart rate.
In the present study, we investigated the effect
of a single bolus administration of L-NAME on
blood pressure and heart rate monitored for one
hour in anesthetized rats and the influence of
vagotomy and b1-receptor blocker metoprolol on
the
L-NAME induced bradycardia. After L-NAME
treatment, the blood pressure rose immediately
after the injection of the drug (peak response in
the third minute: +24 %, p<0.001) and fell to
the control level in the 20th minute. The heart
rate decreased immediately after L-NAME
administration, the lowest value being reached in
the 10th minute (-14 %, p<0.001). However,
bradycardia was sustained even after the blood
pressure had returned to the control level.
Bilateral vagotomy failed to influence the
negative chronotropic effect of L-NAME, but
bradycardia was completely abolished by
metoprolol pretreatment. We concluded that the
bradycardia evoked by L-NAME is mainly due to the
withdrawal of sympathetic tone upon the heart
rate. However, the cause of sustained bradycardia
after normalization of blood pressure cannot be
elucidated.
Key
words
Nitric
oxide · Vagotomy · Metoprolol · Heart rate
Reprint
requests
János Vág, Semmelweis University, Department of
Conservative Dentistry, 1088 Mikszáth K. tér 5,
P.O.Box 124,
H-1431 Budapest, Hungary, Fax: +36-1-317-1122,
e-mail: vag@konfog.sote.hu
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