NOS inhibition blunts and delays the compensatory dilation in hypoperfused contracting human muscles

Darren P Casey; Michael J Joyner

doi:10.1152/japplphysiol.00680.2009

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NOS inhibition blunts and delays the compensatory dilation in hypoperfused contracting human muscles

Journal article

Open access

Peer reviewed

NOS inhibition blunts and delays the compensatory dilation in hypoperfused contracting human muscles

Darren P Casey and Michael J Joyner

Journal of applied physiology (1985), Vol.107(6), pp.1685-1692

12/2009

DOI: 10.1152/japplphysiol.00680.2009

PMCID: PMC2793197

PMID: 19729589

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Abstract

We previously demonstrated that skeletal muscle blood flow is restored in the exercising forearm during experimental hypoperfusion via local dilator and/or myogenic mechanisms. This study examined the role of nitric oxide (NO) in the restoration of blood flow to the active muscles during hypoperfusion. Eleven healthy subjects (10 men/1 woman; 25 +/- 1 yr of age) performed rhythmic forearm exercise (10% and 20% of maximum) while hypoperfusion was evoked by balloon inflation in the brachial artery above the elbow. Each trial included baseline, exercise, exercise with inflation, and exercise after deflation (3 min each). Forearm blood flow (FBF; ultrasound) and local (brachial artery catheter pressure, BAP) and systemic arterial pressure [mean arterial pressure (MAP); Finometer] were measured. The exercise bouts were repeated during N(G)-monomethyl-L-arginine (L-NMMA) infusion (NO synthase inhibition). Forearm vascular conductance (FVC; ml x min(-1) x 100 mmHg(-1)) was calculated from BF (ml/min) and BAP (mmHg). FBF and FVC fell acutely with balloon inflation during all trials (P < 0.01). Recovery of FBF and FVC [(inflation - nadir)/(steady-state exercise - nadir)] with L-NMMA administration was reduced during 20% exercise (FBF = 77 +/- 7% vs. 88 +/- 8%; FVC = 71 +/- 8% vs. 90 +/- 9%; P < 0.01) but not 10% exercise (FBF = 83 +/- 4% vs. 81 +/- 5%, P = 0.37; FVC = 75 +/- 10% vs. 76 +/- 7%; P = 0.44) compared with the respective control trial. The time to steady-state vasodilator response was substantially longer during the l-NMMA trials (10% = 74 +/- 4 s vs. 61 +/- 6 s; 20% = 53 +/- 4 s vs. 41 +/- 4 s; P < 0.05). Thus the magnitude and timing of the NO contribution to compensatory dilation during forearm exercise with hypoperfusion was dependent on exercise intensity. These observations suggest that NO is released by contracting muscles or that a portion of the dilation caused by ischemic metabolites is NO dependent.

Motor Activity - physiology

Acetylcholine - pharmacology

Muscarinic Agonists - pharmacology

Humans

Enzyme Inhibitors - pharmacology

Brachial Artery - metabolism

Male

Muscle, Skeletal - metabolism

omega-N-Methylarginine - pharmacology

Heart Rate - drug effects

Regional Blood Flow - drug effects

Muscle Contraction - drug effects

Muscle, Skeletal - drug effects

Forearm - blood supply

Signal Processing, Computer-Assisted

Adult

Female

Blood Pressure - drug effects

Nitric Oxide Synthase - metabolism

Forearm - physiology

Vasodilation - drug effects

Blood Flow Velocity - drug effects

Brachial Artery - physiology

Muscle, Skeletal - blood supply

Details

Title: Subtitle: NOS inhibition blunts and delays the compensatory dilation in hypoperfused contracting human muscles
Creators: Darren P Casey - Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota 55905, USA. casey.darren@mayo.edu
Michael J Joyner
Resource Type: Journal article
Publication Details: Journal of applied physiology (1985), Vol.107(6), pp.1685-1692
DOI: 10.1152/japplphysiol.00680.2009
PMID: 19729589
PMCID: PMC2793197
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: 12/2009
Academic Unit: Physical Therapy and Rehabilitation Science; Fraternal Order of Eagles Diabetes Research Center
Record Identifier: 9984047786102771

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