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• W2156543149 abstract "Cardiovascular diseases are characterized by insulin resistance and elevated endothelin (ET)-1 levels. Furthermore, ET-1 induces insulin resistance. To elucidate this mechanism, six healthy subjects were studied during a hyperinsulinemic euglycemic clamp during infusion of (the ET-1 precursor) big ET-1 alone or after ET A - or ET B -receptor blockade. Insulin levels rose after big ET-1 with or without the ET B antagonist BQ-788 ( P < 0.05) but were unchanged after the ET A antagonist BQ-123 + big ET-1. Infused glucose divided by insulin fell after big ET-1 with or without BQ-788 ( P < 0.05). Insulin and infused glucose divided by insulin values were normalized by ET A blockade. Mean arterial blood pressure rose during big ET-1 with or without BQ-788 ( P < 0.001) but was unchanged after BQ-123. Skeletal muscle, splanchnic, and renal blood flow responses to big ET-1 were abolished by BQ-123. ET-1 levels rose after big ET-1 ( P< 0.01) in a similar way after BQ-123 or BQ-788, despite higher elimination capacity after ET A blockade. In conclusion, ET-1-induced reduction in insulin sensitivity and clearance as well as splanchnic and renal vasoconstriction are ET A mediated. ET A -receptor stimulation seems to inhibit the conversion of big ET-1 to ET-1." @default.
• W2156543149 created "2016-06-24" @default.
• W2156543149 creator A5051896610 @default.
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• W2156543149 date "2002-12-01" @default.
• W2156543149 modified "2023-10-14" @default.
• W2156543149 title "Insulin sensitivity and big ET-1 conversion to ET-1 after ET_A- or ET_B-receptor blockade in humans" @default.
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• W2156543149 doi "https://doi.org/10.1152/japplphysiol.00477.2002" @default.
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