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Insulin Inhibits Low Oxygen‐Induced ATP Release from Human Erythrocytes: Implication for Vascular Control
Author(s) -
HANSON MADELYN S.,
ELLSWORTH MARY L.,
ACHILLEUS DAVID,
STEPHENSON ALAN H.,
BOWLES ELIZABETH A.,
SRIDHARAN MEERA,
ADDERLEY SHAQURIA,
SPRAGUE RANDY S.
Publication year - 2009
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1080/10739680902855218
Subject(s) - skeletal muscle , insulin , medicine , endocrinology , hyperinsulinemia , vasodilation , chemistry , mastoparan , biology , insulin resistance , receptor , g protein
Objective: ATP released from human erythrocytes in response to reduced oxygen tension (pO 2 ) participates in the matching of oxygen (O 2 ) supply with need in skeletal muscle by stimulating increases in blood flow to areas with increased O 2 demand. Here, we investigated the hypothesis that hyperinsulinemia inhibits ATP release from erythrocytes and impairs their ability to stimulate dilation of isolated arterioles exposed to decreased extraluminal pO 2 . Materials andMethods: Erythrocyte ATP release was stimulated pharmacologically (mastoparan 7) and physiologically (reduced pO 2 ) in the absence or presence of insulin. We also examined the ability of isolated skeletal muscle arterioles perfused with buffer containing erythrocytes treated with insulin or its vehicle (saline) to dilate in response to decreased extraluminal pO 2. Results: Insulin significantly attenuated mastoparan 7– and reduced pO 2 –induced ATP release. In vessels perfused with untreated erythrocytes, low extraluminal pO 2 resulted in an increase in vessel diameter. In contrast, when erythrocytes were treated with insulin, no vasodilation occurred. Conclusions: These studies demonstrate that insulin inhibits ATP release from erythrocytes in response to reduced pO 2 and impairs their ability to stimulate dilation of skeletal muscle arterioles. These results suggest that hyperinsulinemia could hinder the matching of O 2 supply with need in skeletal muscle.