HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Free Full Text (PDF) Free All Versions of this Article: 95/6/2370    most recent 00634.2003v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Rosenmeier, J. B. Articles by Joyner, M. J. Search for Related Content PubMed PubMed Citation Articles by Rosenmeier, J. B. Articles by Joyner, M. J.

Exogenous NO administration and -adrenergic vasoconstriction in human limbs

Department of Anesthesiology and General Clinical Research Center, Mayo Clinic and Foundation, Rochester, Minnesota 55905

Submitted 18 June 2003 ; accepted in final form 11 August 2003

Nitric oxide (NO) is capable of blunting -adrenergic vasoconstriction in contracting skeletal muscles of experimental animals (functional sympatholysis). We therefore tested the hypothesis that exogenous NO administration can blunt -adrenergic vasoconstriction in resting human limbs by measuring forearm blood flow (FBF; Doppler ultrasound) and blood pressure in eight healthy males during brachial artery infusions of three -adrenergic constrictors (tyramine, which evokes endogenous norepinephrine release; phenylephrine, an ₁-agonist; and clonidine, an ₂-agonist). To simulate exercise hyperemia, the vasoconstriction caused by the -agonists was compared during adenosine-mediated (>50% NO independent) and sodium nitroprusside-mediated (SNP; NO donor) vasodilation of the forearm. Both adenosine and SNP increased FBF from 35–40 to 200–250 ml/min. All three -adrenergic constrictor drugs caused marked reductions in FBF and calculated forearm vascular conductance (P < 0.05). The relative reductions in forearm vascular conductance caused by the -adrenergic constrictors during SNP infusion were similar (tyramine, –74 ± 3 vs. –65 ± 2%; clonidine, –44 ± 6 vs. –44 ± 6%; P > 0.05) or slightly greater (phenylephrine, –47 ± 6 vs. –33 ± 6%; P < 0.05) compared with the responses during adenosine. In conclusion, these results indicate that exogenous NO sufficient to raise blood flow to levels simulating those seen during exercise does not blunt -adrenergic vasoconstriction in the resting human forearm.

functional sympatholysis; sympathetic nervous system; sympathetic modulation; nitric oxide

This article has been cited by other articles:

				D. S. Goldstein Genotype and Vascular Phenotype Linked by Catecholamine Systems Circulation, January 29, 2008; 117(4): 458 - 461. [Full Text] [PDF]

				P. J Fadel, Z. Wang, H. Watanabe, D. Arbique, W. Vongpatanasin, and G. D Thomas Augmented sympathetic vasoconstriction in exercising forearms of postmenopausal women is reversed by oestrogen therapy J. Physiol., December 15, 2004; 561(3): 893 - 901. [Abstract] [Full Text] [PDF]

				G. D. Thomas and S. S. Segal Neural control of muscle blood flow during exercise J Appl Physiol, August 1, 2004; 97(2): 731 - 738. [Abstract] [Full Text] [PDF]

				L. B. Rowell Ideas about control of skeletal and cardiac muscle blood flow (1876-2003): cycles of revision and new vision J Appl Physiol, July 1, 2004; 97(1): 384 - 392. [Abstract] [Full Text] [PDF]

				J. B. Rosenmeier, J. Hansen, and J. Gonzalez-Alonso Circulating ATP-induced vasodilatation overrides sympathetic vasoconstrictor activity in human skeletal muscle J. Physiol., July 1, 2004; 558(1): 351 - 365. [Abstract] [Full Text] [PDF]