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- W1121301 abstract "Nitric oxide (NO) contributes to compensatory vasodilation in the contracting human forearm subjected to hypoperfusion during exercise. We tested the potential for adenosine/NO interaction in the compensatory dilation. Eight males (25 ± 2 yrs) performed forearm exercise (20% of max) during intra-arterial balloon inflation. Each trial included; exercise, exercise with balloon inflation, and exercise after deflation (3 min each). Forearm blood flow (FBF; ultrasound) and brachial artery catheter pressure (BAP) were measured. Exercise was repeated during NO synthase inhibition (L-NMMA) alone and with the combination of L-NMMA/aminophylline (adenosine receptor blockade). Forearm vascular conductance (FVC; ml/min/100mmHg) was calculated from BF (ml/min) and BAP (mmHg). The % recovery in FVC during inflation was calculated as (steady state inflation plus exercise value – nadir)/[steady state exercise (control) value-nadir]. FVC fell acutely with balloon inflation during all trials (P < 0.01). During the control trial, the % recovery in FVC was 111 ± 8%. The % recovery in FVC was attenuated with NOS inhibition alone (80 ± 9%; P < 0.001 vs. control) and attenuated further with combined inhibition of NO/adenosine (63 ± 9%; P < 0.05 vs. L-NMMA). Thus, adenosine has an NO independent role in the compensatory vasodilatation during exercise with acute hypoperfusion. NIH HL46493 (MJJ), AR55819 (DPC) and RR-024150." @default.
- W1121301 created "2016-06-24" @default.
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- W1121301 date "2010-04-01" @default.
- W1121301 modified "2023-09-25" @default.
- W1121301 title "Effect of combined inhibition of adenosine and nitric oxide on compensatory vasodilation during exercise with acute hypoperfusion" @default.
- W1121301 doi "https://doi.org/10.1096/fasebj.24.1_supplement.804.10" @default.
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