Key result
ET(A)-receptor blockade with BQ-123 normalized the big ET-1-induced reduction in insulin sensitivity and abolished splanchnic and renal vasoconstriction.
Why the study?
Does ET(A)- or ET(B)-receptor blockade prevent big ET-1-induced insulin resistance and vasoconstriction in healthy subjects?
Population
6 healthy subjects
Comparison
Infusion of big ET-1 alone or after ET-receptor… vs Comparisons between big ET-1 alone, big ET-1 +…
Design
Other
Authors
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ET(A) blockade may offset ET-1 effects on insulin sensitivity and vasoconstriction in healthy subjects; leaves open translation to cardiometabolic disease.
Does ET(A)- or ET(B)-receptor blockade prevent big ET-1-induced insulin resistance and vasoconstriction in healthy subjects?
p-value: p=<0.05
ET-1-induced reduction in insulin sensitivity and clearance, as well as splanchnic and renal vasoconstriction, are mediated by the ET(A) receptor in humans.
Ahlborg et al. (2002) studied Healthy (n=6). ET(A)- or ET(B)-receptor blockade (BQ-123 or BQ-788) prior to big ET-1 infusion vs. big ET-1 alone was evaluated on Insulin sensitivity (infused glucose divided by insulin) (p=<0.05). ET(A)-receptor blockade with BQ-123 normalized the big ET-1-induced reduction in insulin sensitivity and abolished splanchnic and renal vasoconstriction.
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