Key result
Insulin preincubation (120 min) depressed contraction of rat aortic rings to ET1 (132 vs 161 mg/mm2; p<0.05) and AVP, but increased force developed by ET1 in tail arteries.
Why the study?
Does insulin preincubation alter contractile responses to ET1 and AVP in rat aortic and tail artery rings?
Does insulin preincubation alter contractile responses to ET1 and AVP in rat aortic and tail artery rings?
Insulin exerts both vasodilator and vasoconstrictor effects on rat vessels depending on the vascular bed, mediated by endothelial factors.
Vessel bed-specific insulin effects in rats warrant clinical caution; leaves open endothelial mediation in human vessels.
The effect of contractions elicited with ET1 and AVP after preincubating rat aortic and tail artery rings with a hyperinsulinemic dose (3 nM) of insulin were studied. Insulin preincubation (120 min), in the presence of 0.1 mM L-NAME, depressed contraction of aortic rings to 0.01 microM ET1 (132 +/- 6 vs. 161 +/- 9 mg/mm2 in control, n = 25; p < 0.05) and to 1 microM AVP (84 +/- 7 vs. 110 +/- 9 mg/mm2 in control, n = 16; p < 0.05), but did not modify 45Ca influx to the cell. Insulin-induced relaxation was inhibited by indomethacin 10 microM, an antagonist of prostaglandin synthesis, and also by blockade of insulin receptors with 30 microM genistein. A short insulin preincubation (15 min) did not modify ET1 contractions. In rat tail artery, insulin preincubation (120 min) increased the force developed by ET1 (847 +/- 45 vs. 596 +/- 99 mgF/mgW in controls, n = 14) by stimulating TXA2 release and/or actions. In summary, the present results suggest that endothelial factors are involved in both the vasoconstrictor and vasodilator effects of insulin on rat vessels.
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Rebolledo et al. (2001) studied Rat vessel contractile responses. Insulin preincubation vs. Control was evaluated on Contraction of aortic rings to 0.01 microM ET1 (p=<0.05). Insulin preincubation (120 min) depressed contraction of rat aortic rings to ET1 (132 vs 161 mg/mm2; p<0.05) and AVP, but increased force developed by ET1 in tail arteries.
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