Mechanism of coronary vasodilation to insulin and insulin-like growth factor I is dependent on vessel size.
Mechanism of coronary vasodilation to insulin and insulin-like growth factor I is dependent on vessel size.
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DOI：
10.1152/ajpendo.2000.279.1.e176
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发表时间：
2000-07
期刊：
影响因子：
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通讯作者：
C. Oltman;N. Kane;D. Gutterman;R. S. Bar;K. Dellsperger
中科院分区：
文献类型：
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作者：
C. Oltman;N. Kane;D. Gutterman;R. S. Bar;K. Dellsperger
胰岛素和胰岛素样生长因子I(IGF-I)影响许多代谢和有丝分裂过程；这些激素还具有血管活性。这项研究探讨了胰岛素和IGF-I诱导的犬冠状动脉导管和微血管节段扩张的机制。用前列腺素F(2α)收缩后测定冠脉节段张力。内皮素收缩后测量冠脉微血管内径(静息内径=112.6±10.1微米)。血管在对照(Krebs)液中孵育，并用N(Omega)-硝基-L-精氨酸(L-NA)、吲哚美辛或K(+)通道抑制剂处理。缩窄后给予胰岛素或胰岛素样生长因子-I(0.1~100 ng/ml)。在导管动脉，胰岛素产生适度的最大松弛(32+/-5%)，而IGF-I(66+/-12%)。一氧化氮合酶(NOS)和环氧合酶抑制血管扩张，KCl收缩阻断血管扩张。L钠、消炎痛、四乙基氯化铵、格列本脲、白花蛇毒和阿帕明不改变冠脉微血管对胰岛素和胰岛素样生长因子-I的松弛作用，但四丁基氯化铵可减弱这一反应。综上所述，胰岛素和IGF-I可引起犬冠状动脉导管动脉和微血管的扩张。在导管血管中，一氧化氮合酶/环氧合酶通路参与了血管扩张。在微血管中，对胰岛素和IGF-I的松弛不是通过一氧化氮合酶/环氧合酶途径，而是通过K(+)依赖的机制。
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 PGF(2alpha). Internal diameter of coronary microvessels (resting diameter = 112.6+/-10.1 microm) was measured after endothelin constriction. Vessels were incubated in control (Krebs) solution and were treated with N(omega)-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.