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36) amide on arterial blood pressure in
rats
1 Department of Biochemistry and Molecular Biology, University of Salamanca, 37007 Salamanca, Spain; 2 Department of Medicine, Veterans Affairs Medical Center, Bronx, New York 10468; and 3 Department of Biochemistry and Molecular Biology, Faculty of Medicine, Complutense University, 28040 Madrid, Spain
This study was
designed to determine the contribution of the central nervous system
(CNS) to the effects of glucagon-like peptide-1-(7
36) amide (tGLP-1)
on arterial blood pressure and heart rate in rats. Accordingly,
intracerebroventricular administration of the peptide produced an
increase in cardiovascular parameters, which was blocked by previous
administration of exendin-(939) through the same route, but not when
it was intravenously injected. Intravenous administration of tGLP-1
produced a significant increase in arterial blood pressure and heart
rate, which was blocked by the previous intracerebroventricular or
intravenous administration of exendin-(939). Bilateral
vagotomy blocked the stimulating effect of intracerebroventricular
tGLP-1 administration on arterial blood pressure and heart rate. Also,
bilateral vagotomy prevented the blocking effect of
intracerebroventricular but not of intravenous exendin-(939) on
cardiovascular parameters after intravenous administration of tGLP-1.
These findings suggest that the action of tGLP-1 on cardiovascular
parameters is under a dual control generated in the CNS and in
peripheral structures and that the neural information emerging in the
brain is transmitted to the periphery through the vagus nerve.
cardiovascular parameters; neural control; vagal mediation
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