Adenosine does not vasodilate skeletal muscle arterioles via secondary nitric oxide or prostaglandin production

Abstract

We have recently shown that ADO is responsible for arteriolar vasodilation in response to skeletal muscle contraction. To determine whether the arteriolar vasodilation induced by adenosine (ADO) is, in part, due to the production of nitric oxide and prostaglandins we stimulated transverse arterioles (approx. 40μm) in a hamster cremaster preparation with a range of concentrations of ADO (10−7–10−5M) and measured the diameter of arterioles in the absence of and in the presence of cyclooxygenase inhibitor indomethacin (10−6M INDO), or nitric oxide synthase inhibitor L‐NAME (10−6M), or both. We further investigated whether there was an inhibition of ADO dilation in the presence of L‐NAME and nitric oxide donor SNAP (10−7M). We observed significant vasodilation at all concentrations of ADO (change in diameter with 10−7M ADO:4.8±1.0μm, 10−6M: 11.5±1.5μm, 5×10−6M:18.9±1.7μm, 10−7M: 22.0±1.5μm) that were not significantly inhibited by INDO or L‐NAME, or INDO plus L‐NAME. Further, supplementation of the L‐NAME inhibition with SNAP did not alter any vasodilation induced by ADO. These findings show that ADO does not cause vasodilation through the production of nitric oxide or prostaglandins. These data indicate that the ADO involved in arteriolar vasodilation in response to muscle contraction is not responsible for producing secondary vasodilators such and nitric oxide or prostaglandins.