INVESTIGADORES
MAYER Marcos Alejandro
artículos
Título:
Oral treatment and in vitro incubation with fructose modify vascular prostanoid production in the rat
Autor/es:
H.A. PEREDO; M.A. MAYER; M. RODRÍGUEZ FERMEPÍN; D. GRINSPON; A.M. PUYÓ
Revista:
Autonomic & Autacoid Pharmacology
Referencias:
Año: 2006 vol. 26 p. 15 - 20
Resumen:
1.In the rat, a fructose-enriched diet induces hyperglycaemia,
hypertriglyceridaemia, insulin resistance and hypertension; a model
which resembles the human metabolic syndrome. 2.-- Prostanoids,
metabolites of arachidonic acid, include vasoactive substances
synthesized and released from the vascular wall that have been
implicated in the increase of peripheral resistance, one of the
mechanisms involved in the fructose-induced hypertension. 3.-- The aim
of the present study was to: (i) analyse the effects of the in vitro
incubation with fructose on the production and release of prostanoids
in rat thoracic aorta and in rat mesenteric bed and (ii) compare the
effects of incubation with those of the in vivo acute and chronic
treatment of rats with fructose and with the combination of both in
vivo and in vitro procedures. 4.-- Blood pressure, glycaemia and
triglyceridaemia were significantly elevated in both 4- and 22-week
fructose-treated groups. Meanwhile, body and heart weight as well as
insulinaemia were similar between experimental animals and controls.
5.-- In aortae, 4 weeks of Fructose treatment did not modify the
prostanoid pattern release, but in vitro incubation decreased
prostacyclin (PGI(2)) production. However, after 22 weeks, fructose
treatment and incubation exerted the same effect. 6.-- In mesenteric
bed, after 4 weeks, the incubation and the combination of both
procedures reduced the release of the vasodilators PGI(2) and PGE(2),
while fructose treatment only diminished the PGE(2) release. On the
contrary, the production of the vasoconstrictor thromboxane A(2)
(TXA(2)) was enhanced by incubation and both the procedures. After 22
weeks, fructose treatment increased PGI(2) release, while it was
reduced by incubation. The combination of both did not modify this
peripheral resistance when compared with controls. Finally, incubation
of tissues from treated rats increased the release of the
vasoconstrictors, PGF(2alpha) and TXA(2). 7.-- In conclusion, the
mesenteric bed, a resistance vascular bed, seems to be more sensitive
than the aorta, a conductance vessel, to the effects of fructose on
prostanoid production. This difference could be related to a more
relevant role of resistance vessels in the regulation of peripheral
resistance and consequently of blood pressure. The observed effects
should contribute to a shift in the balance of the release of
prostanoid in favour of vasoconstrictor metabolites. This phenomenon
could be related to an increase in the peripheral resistance and the
mild hypertension observed in the fructose-treated rats.