INVESTIGADORES
MAYER Marcos Alejandro
artículos
Título:
Fructose overload modifies vascular morphology and prostaglandin production in rats
Autor/es:
A.M. PUYÓ; M.A. MAYER; S. CAVALLERO; A.S. DONOSO; H.A. PEREDO
Revista:
Autonomic & Autacoid Pharmacology
Referencias:
Año: 2004 vol. 24 p. 29 - 35
Resumen:
1. A fructose (Fru)-enriched diet induces a mild increase in blood
pressure associated with hyperglycaemia, hypertriglyceridaemia, and
insulin resistance, resembling the human 'syndrome X', being an useful
model to study hypertension and type 2 diabetes. 2. A sustained
elevation of blood pressure is associated with cardiovascular
structural modifications such as left ventricular hypertrophy and
increased wall thickness:lumen diameter ratio in blood vessels. 3.
Prostanoids (PR), metabolites of arachidonic acid through the
cyclooxygenase pathway, include vasoactive substances synthesized and
released by the vessel walls. 4. The aim of the present study was to
analyse, in Fru-treated rats: (i) the morphology of mesenteric vessels
and; (ii) the PR production in aorta and mesenteric vessels, in order
to assess whether these parameters are related with the haemodynamic
alterations observed in this experimental model. 5. Blood pressure,
glycaemia and triglyceridaemia, were significantly elevated in both (4
and 22 weeks) Fru-treated groups. Meanwhile body and heart weight as
well as insulinaemia were similar between experimental animals and
controls. 6. The mesenteric vessels of Fru-treated rats (22 weeks)
showed an increased thickness and area of the media when compared with
the controls; meanwhile, the lumen diameter was similar in both groups.
7. The Fru treatment for 4 weeks did not modify PR production in aorta,
whereas in the mesenteric bed it diminished prostaglandin (PG) E(2)
release significantly compared with the controls. However, in the group
treated for 22 weeks, Fru reduced PGI(2) production in the aorta, as
assessed by 6-keto-PGF(1)alpha measurements. Meanwhile, in the
mesenteric bed, the chronic Fru treatment decreased PGE(2) release but,
rather surprisingly, increased the output of PGI(2) when compared with
its corresponding controls. 8. In conclusion, the present study shows
the existence of an alteration in the morphology of mesenteric vessels
in Fru-treated rats, which could be related to an increase in
peripheral resistance and the consequent mild hypertension observed in
this model. However, a diminished release of vasodilator PRs, such as
PGE(2) in mesenteric vessels at 4 and 22 weeks and PGI(2) in aorta at
22 weeks could further impair the vessel response. The increase in
PGI(2) observed in the chronic group in mesenteric vessels could be
attributed to a compensatory mechanism.