Vascular and neural mechanisms of ACh-mediated vasodilation in the forearm cutaneous microcirculation

The relative contribution of endothelial vasodilating factors to acetylcholine (ACh)-mediated vasodilation in the forearm cutaneous microcirculation is unclear. The aims of this study were to investigate the contributions of prostanoids and cutaneous C fibers to basal cutaneous blood flow (CuBF) and...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of applied physiology (1985) Jg. 92; H. 2; S. 780
Hauptverfasser: Berghoff, Martin, Kathpal, Madeera, Kilo, Sonja, Hilz, Max J, Freeman, Roy
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 01.02.2002
Schlagworte:
Acetylcholine - pharmacology
Acetylcholine - physiology
Adult
Axons - physiology
Blood Vessels - innervation
Dose-Response Relationship, Drug
Electric Stimulation
Female
Forearm - blood supply
Forearm - innervation
Humans
Iontophoresis
Lidocaine - pharmacology
Male
Microcirculation - drug effects
Microcirculation - physiology
Prilocaine - pharmacology
Reflex - physiology
Regional Blood Flow - drug effects
Sensation - drug effects
Sensation - physiology
Skin - blood supply
Vasodilation - physiology
Vasodilator Agents - administration & dosage
Vasodilator Agents - pharmacology
ISSN:8750-7587
Online-Zugang:Weitere Angaben
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:The relative contribution of endothelial vasodilating factors to acetylcholine (ACh)-mediated vasodilation in the forearm cutaneous microcirculation is unclear. The aims of this study were to investigate the contributions of prostanoids and cutaneous C fibers to basal cutaneous blood flow (CuBF) and ACh-mediated vasodilation. ACh was iontophoresed into the forearm, and cutaneous perfusion was measured by laser-Doppler flowmetry. To inhibit the production of prostanoids, four doses of acetylsalicylic acid (ASA; 81, 648, 972, and 1,944 mg) were administered orally. Cutaneous nerve fibers were blocked with topical anesthesia. Cyclooxygenase inhibition did not change basal CuBF or endothelium-mediated vasodilation to ACh. In contrast, ASA (972 and 1,944 mg) significantly reduced the C-fiber-mediated axon reflex in a dose-dependent fashion. Blockade of C-fiber function significantly reduced axon reflex-mediated vasodilation but did not affect basal CuBF or endothelium-dependent vasodilation. The findings suggest that prostanoids do not contribute significantly to basal CuBF or endothelium-dependent vasodilation in the forearm microcirculation. In contrast, prostanoids are mediators of the ACh-provoked axon reflex.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:8750-7587
DOI:10.1152/japplphysiol.01167.2000