(Circulation. 1996;93:1403-1410.)
© 1996 American Heart Association, Inc.
Articles |
Insulin Modulation of ß-Adrenergic Vasodilator Pathway in Human Forearm
From the Istituto Neurologico Mediterraneo, Neuromed, Pozzilli (IS) (G.L., C.V., B.T.), and the Department of Internal Medicine, School of Medicine, Federico II University, Naples (G.I., V.R., L.P., B.T.), Italy.
Correspondence to Bruno Trimarco, MD, Medicina Interna, Università di Napoli Federico II, Via S Pansini 5, 80131 Napoli, Italy. E-mail trimarco@ds.cised.unina.it.
Background Insulin modulates sympathetic
vasoconstriction, but the mechanisms underlying this effect are not
completely elucidated. We have recently investigated the insulin effect
on the 
1- and 2-adrenergic
vasoconstriction pathway, where it is still conflicting with the
possible insulin influence on the ß-adrenergic vasodilator
pathway. The aim of the present study was to investigate this
issue.
Methods and Results The study was performed on the forearm
of healthy humans, and all test substances were infused into the
brachial artery at systemically ineffective rates. In five subjects, we
evaluated isoproterenol-induced vasodilation (1, 3, 6, and 9
ng·kg-1·min-1)
both under control conditions and during insulin infusion (0.05
mU·kg-1·min-1).
In another group of five subjects, we tested whether the vasorelaxant
effect of sodium nitroprusside (1, 2, 4, and 8
ng·kg-1·min-1)
was modified by insulin. Moreover, to explore whether the interaction
between insulin and forearm ß-adrenergic pathway participates in
insulin modulation of sympathetic-evoked vasoconstriction, we
measured in six normal subjects the forearm vascular response to
lower-body negative pressure under control conditions and during
intrabrachial infusion of insulin alone and in combination with a
selective ß-adrenergic blocking agent (propranolol 10
µg/100 mL per minute). Finally, to verify whether insulin interaction
with the ß-adrenergic pathway may also account for insulin
modulation of 2-adrenergic vasoconstriction, we assessed
the vascular response to a selective 2-adrenergic
agonist before and after propranolol administration.
Insulin exposure potentiated the vascular responsiveness to
isoproterenol but did not affect the vasodilator response to sodium
nitroprusside. Furthermore, the insulin-induced attenuation of
sympathetic vasoconstriction was partially corrected by
propranolol. In contrast, the insulin modulation of
2-adrenergic vasoconstriction was not influenced by
ß-adrenergic blockade.
Conclusions Taken together, our results suggest that
insulin modulation of sympathetic-induced vasoconstriction is
carried out through an interaction of the hormone with the pathways of
both 2- and ß-adrenergic receptors.
Key Words: forearm vascular resistance • nervous system • receptors, adrenergic, alpha
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