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• W2073669830 abstract "Objective: In the vasculature insulin activates two distinct signaling pathways that result in secretion of nitric oxide (NO) and endothelin (ET-1), respectively. NO, stimulated by higher insulin doses, is thought to be the underlying agent in insulin-mediated, endothelium-dependent vasodilation. However, we have shown that at low doses insulin causes vasoconstriction in the human microcirculation. We postulated that ET-1 stimulated by insulin could be responsible for this vasoconstriction. In an earlier study we found, that insulin at a dose, that by itself caused vasoconstriction, inhibited vasodilation to an ET-1-type-A-receptor (ET-A)-antagonist, suggesting increased insulin-mediated ET-1-activity. The role of ET-1-type-B (ET-B)-receptors in this setting remained to be identified and was the focus of the present study. Methods: 18 healthy women and men (25 ± 4 years) were studied. We used a Laser-Doppler-Imager (moor LDI-V5.0, Axminister,UK) to measure changes in skin blood flow. 10-7 IU insulin (Insuman Rapid®, Sanofi,Germany) were injected intradermally alone or following injection of the ET-A-antagonist BQ123 10-8 mol, the ET-B-antagonist BQ788 10-8 mol (Bachem,Switzerland) and BQ123 10–8+BQ788 10–8 mol in combination. Effects of BQ123 10–8 mol and BQ788 (10–8 and 10–10 mol) were also recorded. Injection sites were scanned over 30 min. Data are presented as arbitrary perfusion units (PU) and are given as mean ± SD. Two-way ANOVA was used to analyze time-effect responses. Results: Again insulin led to mild but significant vasoconstriction (P < 0.0001 vs. baseline) and reduced BQ123-mediated vasodilation (BQ123 vs. BQ123+insulin: +177 ± 60 vs. +87 ± 39PU, P < 0.0001). ET-B-blockade with BQ788 at the lower dose (10–10 mol) produced vasoconstriction (−24 ± 8PU, P < 0.0001 vs. baseline), which at the higher dose (10–8 mol) was no longer present. In the presence of ET-B-blockade (BQ788 10–8 mol) insulin induced vasodilation (+104 ± 32PU, P < 0.0001 vs. baseline). Blockade of both ET-A and ET-B-receptors induced pronounced vasodilation that was not different from vasodilation to ET-A-blockade alone. However, in the presence of BQ788 insulin no longer affected vasodilation induced by BQ123. Conclusions: Vasoconstrictor effects of low insulin doses in the peripheral microcirculation of healthy humans seem to be mediated via ET-B-receptors." @default.
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• W2073669830 date "2010-06-01" @default.
• W2073669830 modified "2023-09-24" @default.
• W2073669830 title "VASOCONSTRICTOR EFFECTS OF INSULIN IN THE HUMAN MICROCIRCULATION ARE MEDIATED VIA ENDOTHELIN-1-TYPE-B-RECEPTORS: 3D.04" @default.
• W2073669830 doi "https://doi.org/10.1097/01.hjh.0000378316.16854.7f" @default.
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