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Vol. 282, Issue 2, 691-698, 1997
-Triphosphate and Noradrenaline as Sympathetic
Cotransmitters in the Rat Arterial Mesenteric
Bed1
Unidad de Regulación Neurohumoral, Departamento de Ciencias
Fisiológicas, Facultad de Ciencias Biológicas, P. Universidad Católica de Chile, Casilla 114-D, Santiago, Chile
The physiological role of neuropeptide Y (NPY) and extracellular
adenosine 5
-triphosphate (ATP) in sympathetic neurotransmission is
becoming increasingly clear. To assess whether NPY and ATP act as
cotransmitters together with noradrenaline (NA) in the sympathetic
nerves of the superior mesenteric artery, the changes in perfusion
pressure of the arterial mesenteric bed caused by nerve stimulation
were recorded. Depolarization of the perivascular superior mesenteric
arterial nerves caused frequency- and time-dependent increases in the
perfusion pressure that were abolished by guanethidine, which implied
the sympathetic origin of these responses. Independent perfusion with
either 500 nM BIBP 3226, an NPY Y1 antagonist; 3 µM suramin, a competitive purinoceptor antagonist; or 0.1 nM prazosin, a competitive alpha-1 adrenoceptor antagonist,
evoked approximately a 30% reduction in the rise in perfusion pressure caused by the 20- to 30-Hz electrical depolarization of the
perimesenteric arterial nerves. Prazosin (0.1 nM) blocked the increases
in perfusion pressure caused by electrical stimulation of the
perimesenteric nerves but did not significantly reduce the vasomotor
effect of exogenous NA. Likewise, 5-methyl urapidil and
chloroethylclonidine, alpha-1 adrenoceptor antagonists with
selectivity for the alpha-1A and alpha-1B
receptor subtypes, respectively, concentration-dependently decreased
the increase in perfusion pressure elicited by electrical stimulation
of the perimesenteric nerves at concentrations lower than that required
to block the vasoconstriction elicited by exogenous NA. The combined
perfusion of 3 µM suramin plus 0.1 nM prazosin did not result in a
complete inhibition of the physiological response. Only upon the
simultaneous application of BIBP plus suramin plus prazosin was the
rise in perfusion pressure abolished. These results support the working
hypothesis that the sympathetic nerves of the rat mesenteric bed
release NPY, ATP and NA that act as postjunctional cotransmitters in
this neuroeffector junction.
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