Contribution of adenosine to compensatory dilation in hypoperfused contracting human muscles is independent of nitric oxide

Darren P Casey; Michael J Joyner

doi:10.1152/japplphysiol.00836.2010

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Contribution of adenosine to compensatory dilation in hypoperfused contracting human muscles is independent of nitric oxide

Journal article

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Contribution of adenosine to compensatory dilation in hypoperfused contracting human muscles is independent of nitric oxide

Darren P Casey and Michael J Joyner

Journal of applied physiology (1985), Vol.110(5), pp.1181-1189

05/2011

DOI: 10.1152/japplphysiol.00836.2010

PMCID: PMC3098657

PMID: 21292838

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Abstract

We previously demonstrated that nitric oxide (NO) contributes to compensatory vasodilation in the contracting human forearm subjected to acute hypoperfusion. We examined the potential role of an adenosine-NO interaction to this response in 17 male subjects (25 ± 2 yr). In separate protocols subjects performed rhythmic forearm exercise (20% of maximum) while hypoperfusion was evoked by balloon inflation in the brachial artery above the elbow. Each trial included exercise before inflation, exercise with inflation, and exercise after deflation (3 min each). Forearm blood flow (FBF; ultrasound) and local [brachial artery catheter pressure (BAP)] and systemic [mean arterial pressure (MAP); Finometer] arterial pressure were measured. In protocol 1 (n = 10), exercise was repeated during nitric oxide synthase inhibition [N(G)-monomethyl-L-arginine (L-NMMA)] alone and during L-NMMA-aminophylline (adenosine receptor blockade) administration. In protocol 2, exercise was repeated during aminophylline alone and during aminophylline-L-NMMA. Forearm vascular conductance (FVC; ml·min(-1)·100 mmHg(-1)) was calculated from blood flow (ml/min) and BAP (mmHg). Percent recovery in FVC during inflation was calculated as (steady-state inflation + exercise value - nadir)/[steady-state exercise (control) value - nadir]. In protocol 1, percent recovery in FVC was 108 ± 8% during the control (no drug) trial. Percent recovery in FVC was attenuated with inhibition of NO formation alone (78 ± 9%; P < 0.01 vs. control) and was attenuated further with combined inhibition of NO and adenosine (58 ± 9%; P < 0.01 vs. L-NMMA). In protocol 2, percent recovery was reduced with adenosine receptor blockade (74 ± 11% vs. 113 ± 6%, P < 0.01) compared with control drug trials. Percent recovery in FVC was attenuated further with combined inhibition of adenosine and NO (48 ± 11%; P < 0.05 vs. aminophylline). Our data indicate that adenosine contributes to compensatory vasodilation in an NO-independent manner during exercise with acute hypoperfusion.

Muscle Contraction

Physical Exertion - physiology

Humans

Adaptation, Physiological - physiology

Adenosine - metabolism

Adult

Male

Muscle, Skeletal - physiology

Vasodilation - physiology

Nitric Oxide - metabolism

Blood Flow Velocity - physiology

Details

Title: Subtitle: Contribution of adenosine to compensatory dilation in hypoperfused contracting human muscles is independent of nitric oxide
Creators: Darren P Casey - Department of Anesthesiology, Mayo Clinic Rochester, MN 55905, USA. casey.darren@mayo.edu
Michael J Joyner
Resource Type: Journal article
Publication Details: Journal of applied physiology (1985), Vol.110(5), pp.1181-1189
DOI: 10.1152/japplphysiol.00836.2010
PMID: 21292838
PMCID: PMC3098657
NLM abbreviation: J Appl Physiol (1985)
ISSN: 8750-7587
eISSN: 1522-1601
Publisher: United States
Grant note: AR-55819 / NIAMS NIH HHS RR-024150 / NCRR NIH HHS HL-46493 / NHLBI NIH HHS
Language: English
Date published: 05/2011
Academic Unit: Physical Therapy and Rehabilitation Science; Fraternal Order of Eagles Diabetes Research Center
Record Identifier: 9984047976202771

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