INVESTIGADORES
MAYER Marcos Alejandro
artículos
Título:
Impaired response to insulin associated to protein kinase C in chronic fructose-induced hypertension.
Autor/es:
P. F. DAMIANO; S. CAVALLERO; M. A. MAYER; M. I. ROSÓN; I. J. DE LA RIVA; B.E. FERNÁNDEZ; A. M. PUYÓ
Revista:
Blood Pressure
Editorial:
Taylor and Francis
Referencias:
Lugar: Göteborg, Suecia; Año: 2002 vol. 11 p. 345 - 351
ISSN:
0803-7051
Resumen:
A fructose-enriched diet induces an increase in blood pressure
associated with metabolic alterations in rats. Our hypothesis was that
an increase in protein kinase C (PKC) activation, reported in the acute
period of fructose overload, and an impaired vessel's response to
vasoactive substances contribute to maintain elevated blood pressure
levels in the chronic period. The aims of this study were to
investigate in this animal model of hypertension: (1) if the increase
in PKC activation was also found in the chronic stage; (2) the
involvement of nitric oxide and insulin in the vessel's response; and
plasma atrial natriuretic factor and nitrites/nitrates (nitric oxide
metabolites) behavior. We evaluated the effects of: PKC-stimulator
12,13-phorbol dibutyrate, phenylephrine, insulin, nitric oxide
synthase-inhibitor NG-nitro-L-arginine methyl esther (L-NAME) and
PKC-inhibitor Calphostin C on aortic rings responses of Sprague-Dawley
rats: fructose-fed and control. The fructose-fed group showed higher
contractility to 12,13-phorbol dibutyrate than the control group in
aortic rings pre-incubated with insulin, and this difference
disappeared with L-NAME. The response to phenylephrine in rings
pre-incubated with Calphostin C was decreased in the fructose-fed group
and increased with Calphostin C plus L-NAME. Fructose-fed rats showed
higher levels of plasma atrial natriuretic factor and nitrites/nitrates
than controls. In conclusion, chronic fructose feeding seems to develop
an impaired response to insulin, dependent on nitric oxide, suggesting
a PKC alteration. Vasorelaxant agents, such as atrial natriuretic
factor and nitric oxide, would behave as compensatory mechanisms in
response to high blood pressure.