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1 Department of Veterans Affairs and 2 Department of Internal Medicine and the Cardiovascular Center, University of Iowa, Iowa City, Iowa 52246
Insulin and insulin-like
growth factor I (IGF-I) influence numerous metabolic and mitogenic
processes; these hormones also have vasoactive properties. This study
examined mechanisms involved in insulin- and IGF-I-induced dilation in
canine conduit and microvascular coronary segments. Tension of coronary
artery segments was measured after constriction with
PGF2
. Internal diameter of coronary microvessels
(resting diameter = 112.6 ± 10.1 µm) was measured after
endothelin constriction. Vessels were incubated in control (Krebs)
solution and were treated with
N
-nitro-L-arginine
(L-NA), indomethacin, or K+ channel inhibitors.
After constriction, cumulative doses of insulin or IGF-I (0.1-100
ng/ml) were administered. In conduit arteries, insulin produced modest
maximal relaxation (32 ± 5%) compared with IGF-I (66 ± 12%). Vasodilation was attenuated by nitric oxide synthase (NOS) and
cyclooxygenase inhibition and was blocked with KCl constriction.
Coronary microvascular relaxation to insulin and IGF-I was not altered
by L-NA, indomethacin, tetraethylammonium chloride,
glibenclamide, charybdotoxin, and apamin; however, tetrabutylammonium chloride attenuated the response. In conclusion, insulin and IGF-I cause vasodilation in canine coronary conduit arteries and
microvessels. In conduit vessels, NOS/cyclooxygenase pathways are
involved in the vasodilation. In microvessels, relaxation to insulin
and IGF-I is not mediated by NOS/cyclooxygenase pathways but rather
through K+-dependent mechanisms.
diabetes mellitus; coronary circulation; coronary microcirculation; dogs; potassium channels
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