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

Darren P. Casey, Michael Joseph Joyner

Research output: Contribution to journalArticle

18 Citations (Scopus)

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 [NG-monomethyl-L-arginine (L-NMMA)] alone and during L-NMMAaminophylline (adenosine receptor blockade) administration. In protocol 2, exercise was repeated during aminophylline alone and during aminophylline-L-NMMA. Forearm vascular conductance (FVC; mlmin -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.

Original languageEnglish (US)
Pages (from-to)1181-1189
Number of pages9
JournalJournal of Applied Physiology
Volume110
Issue number5
DOIs
StatePublished - May 2011

Fingerprint

Adenosine
Economic Inflation
omega-N-Methylarginine
Dilatation
Nitric Oxide
Forearm
Aminophylline
Muscles
Brachial Artery
Purinergic P1 Receptors
Drug and Narcotic Control
Vasodilation
Arterial Pressure
Catheters
Pressure
Elbow
Nitric Oxide Synthase
Blood Vessels
Exercise

Keywords

  • Exercise
  • Hypoperfusion
  • Vasodilation

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Contribution of adenosine to compensatory dilation in hypoperfused contracting human muscles is independent of nitric oxide. / Casey, Darren P.; Joyner, Michael Joseph.

In: Journal of Applied Physiology, Vol. 110, No. 5, 05.2011, p. 1181-1189.

Research output: Contribution to journalArticle

@article{20028077797149698850516fb4d02264,
title = "Contribution of adenosine to compensatory dilation in hypoperfused contracting human muscles is independent of nitric oxide",
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 [NG-monomethyl-L-arginine (L-NMMA)] alone and during L-NMMAaminophylline (adenosine receptor blockade) administration. In protocol 2, exercise was repeated during aminophylline alone and during aminophylline-L-NMMA. Forearm vascular conductance (FVC; mlmin -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.",
keywords = "Exercise, Hypoperfusion, Vasodilation",
author = "Casey, {Darren P.} and Joyner, {Michael Joseph}",
year = "2011",
month = "5",
doi = "10.1152/japplphysiol.00836.2010",
language = "English (US)",
volume = "110",
pages = "1181--1189",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "5",

}

TY - JOUR

T1 - Contribution of adenosine to compensatory dilation in hypoperfused contracting human muscles is independent of nitric oxide

AU - Casey, Darren P.

AU - Joyner, Michael Joseph

PY - 2011/5

Y1 - 2011/5

N2 - 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 [NG-monomethyl-L-arginine (L-NMMA)] alone and during L-NMMAaminophylline (adenosine receptor blockade) administration. In protocol 2, exercise was repeated during aminophylline alone and during aminophylline-L-NMMA. Forearm vascular conductance (FVC; mlmin -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.

AB - 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 [NG-monomethyl-L-arginine (L-NMMA)] alone and during L-NMMAaminophylline (adenosine receptor blockade) administration. In protocol 2, exercise was repeated during aminophylline alone and during aminophylline-L-NMMA. Forearm vascular conductance (FVC; mlmin -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.

KW - Exercise

KW - Hypoperfusion

KW - Vasodilation

UR - http://www.scopus.com/inward/record.url?scp=79956084429&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79956084429&partnerID=8YFLogxK

U2 - 10.1152/japplphysiol.00836.2010

DO - 10.1152/japplphysiol.00836.2010

M3 - Article

VL - 110

SP - 1181

EP - 1189

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 5

ER -