Contributions of acetylcholine and nitric oxide to forearm blood flow at exercise onset and recovery

J. K. Shoemaker, J. R. Halliwill, R. L. Hughson, Michael Joseph Joyner

Research output: Contribution to journalArticle

123 Citations (Scopus)

Abstract

The contributions of acetylcholine and/or nitric oxide (NO) to the rapid changes in human forearm blood flow (FBF) at the onset and recovery from mild exercise were studied in eight subjects. Rhythmic handgrip contractions were performed during brachial artery infusions of saline (2 ml/min; control), atropine (0.2 mg over 3 min), to block acetylcholine binding to muscarinic receptors, or atropine + ATG-monomethyl-Larginine (L-NMMA; 4 mg/min for 4 min), to additionally inhibit NO synthase. Brachial artery mean blood velocity (MBV; pulsed Doppler ultrasound) and diameter (echo Doppler) were measured continuously, and FBF was calculated. Atropine reduced acetylcholine-induced increases in FBF by -71% (P < 0.05). FBF at rest was reduced by atropine and further reduced with atropine + L-NMMA. Both drug conditions reduced FBF during exercise by -10% compared with control, with no difference between drug treatments. Brachial artery diameter was unchanged from rest by exercise, recovery, and drug treatments. Neither drug treatment altered the rate or magnitude of the increase in FBF above rest. Peak FBF after exercise was reduced by atropine and atropine + L-NMMA. Total FBF during 5 min of recovery was reduced with atropine + L-NMMA compared with control and atropine. The results suggest that 1) acetylcholine and NO mechanisms additively contribute to FBF levels at rest, 2) a cholinergic mechanism adjusts the absolute FBF levels during exercise, 3) neither acetylcholine nor NO is essential to observe the normal time course or magnitude of the exercise response, and 4) NO contributes to the FBF response during recovery from exercise. brachial artery; pulsed Doppler; echo Doppler; vasodilation; atropine; A-monomethyl-L-arginine

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume42
Issue number5
StatePublished - 1997

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Forearm
Acetylcholine
Atropine
Nitric Oxide
omega-N-Methylarginine
Brachial Artery
Pharmaceutical Preparations
Doppler Ultrasonography
Muscarinic Receptors
Vasodilation
Nitric Oxide Synthase
Cholinergic Agents
Arginine

ASJC Scopus subject areas

  • Physiology

Cite this

Contributions of acetylcholine and nitric oxide to forearm blood flow at exercise onset and recovery. / Shoemaker, J. K.; Halliwill, J. R.; Hughson, R. L.; Joyner, Michael Joseph.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 42, No. 5, 1997.

Research output: Contribution to journalArticle

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abstract = "The contributions of acetylcholine and/or nitric oxide (NO) to the rapid changes in human forearm blood flow (FBF) at the onset and recovery from mild exercise were studied in eight subjects. Rhythmic handgrip contractions were performed during brachial artery infusions of saline (2 ml/min; control), atropine (0.2 mg over 3 min), to block acetylcholine binding to muscarinic receptors, or atropine + ATG-monomethyl-Larginine (L-NMMA; 4 mg/min for 4 min), to additionally inhibit NO synthase. Brachial artery mean blood velocity (MBV; pulsed Doppler ultrasound) and diameter (echo Doppler) were measured continuously, and FBF was calculated. Atropine reduced acetylcholine-induced increases in FBF by -71{\%} (P < 0.05). FBF at rest was reduced by atropine and further reduced with atropine + L-NMMA. Both drug conditions reduced FBF during exercise by -10{\%} compared with control, with no difference between drug treatments. Brachial artery diameter was unchanged from rest by exercise, recovery, and drug treatments. Neither drug treatment altered the rate or magnitude of the increase in FBF above rest. Peak FBF after exercise was reduced by atropine and atropine + L-NMMA. Total FBF during 5 min of recovery was reduced with atropine + L-NMMA compared with control and atropine. The results suggest that 1) acetylcholine and NO mechanisms additively contribute to FBF levels at rest, 2) a cholinergic mechanism adjusts the absolute FBF levels during exercise, 3) neither acetylcholine nor NO is essential to observe the normal time course or magnitude of the exercise response, and 4) NO contributes to the FBF response during recovery from exercise. brachial artery; pulsed Doppler; echo Doppler; vasodilation; atropine; A-monomethyl-L-arginine",
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