(Hypertension. 2001;37:1480.)
© 2001 American Heart Association, Inc.
Scientific Contributions |
Impaired Insulin-Like Growth Factor I Vasorelaxant Effects in Hypertension
From IRCCS "INM Neuromed" (C.V., S.C., L.F., M.T.G., G.S., G.F., B.T., G.L.), Pozzilli (IS); Department of Internal Medicine, School of Medicine, "Federico II" University (B.T.), Naples; and Departments of Experimental Medicine and Pathology, La Sapienza University (G.L.), Rome, Italy.
Correspondence to Giuseppe Lembo, MD, PhD, IRCCS "INM Neuromed," Località Camerelle, 86077 Pozzilli (IS) Italy. E-mail lembo{at}neuromed.it
Abstract—Insulin-like
growth factor I (IGF-I) can be considered a factor potentially involved
in arterial hypertension not only for its growth-promoting
features but also for its effects on vascular tone. Nevertheless, the
actions of the hormone on vascular reactivity are still unexplored in
hypertension. Therefore, the vasodilation induced by increasing doses
of IGF-I and the modulation of norepinephrine
vasoconstriction induced by low levels of the hormone were tested on
aortic rings of spontaneously hypertensive and normotensive rats. The
results indicate that the vasodilation evoked by IGF-I is impaired in
hypertensive rats (
% of maximal vasorelaxation, 30±1 versus 41±1;
P<0.01), and after the removal
of endothelium or the inhibition of
endothelial NO synthase, the vasodilation evoked by the
hormone was blunted in both rat strains and became similar between
hypertensive and normotensive rats (% of maximal vasorelaxation,
21±1 versus 20±1;
P=NS). Moreover, IGF-I
does not show any effect on norepinephrine vasoconstriction
in hypertensive rats, and this alteration may depend on the lack of
sensitizing effect exerted by IGF-I on
2-adrenergic–evoked NO vasorelaxation. The
defect in IGF-I vascular action is also present in young
spontaneously hypertensive rats (age 5 weeks). In conclusion, our data
demonstrate that IGF-I vasorelaxant properties are impaired in
spontaneously hypertensive rats, suggesting that such defect may play a
causative or permissive role in the development of hypertensive
conditions.
Key Words: vascular reactivity • aorta • norepinephrine • nitric oxide • receptors, adrenergic, alpha
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