Histamine inhibits conducted vasodilation through endothelium‐derived NO production in arterioles of mouse skeletal muscle

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Abstract
Conducted vasodilation along arterioles manifests the spread of hyperpolarization through gap junction channels along endothelium. Whereas histamine increases the permeability of capillary and venular endothelium, its effect on the integrity of arteriolar endothelium is unknown. We tested whether histamine could inhibit conducted vasodilation. In second-order arterioles (2A) supplying the cremaster muscle of C57BL6, PECAM-1−/−, and eNOS−/− mice (8–12 wk), neither resting (16±2 |xm) nor maximal (38±2 µm) diameters were different. Acetylcholine (ACh) microiontophoresis (1 µA, 500 ms pulse) triggered vasodila¬tion that was conducted >1400 µ,πι along arterioles. Neither local (14±2 µπι) nor conducted vasodilation (10±2 µm) was different among mice. Histamine (5 µM) had no effect on resting diameter or local vasodilation to ACh yet inhibited conduction by >50% in C57BL6 and PECAM-1−/− mice (P−/− mice vs. C57BL6 mice. Re¬markably, conducted vasodilation in eNOS−/− mice was insensitive to histamine. These findings indicate that histamine inhibits cell-to-cell coupling through an NO-dependent mechanism and suggests a dynamic interaction among intercellular adhesion molecules and gap junction channels along arteriolar endothelium.—Payne, G. W., Madri, J. A., Sessa, W. C., Segal, S. S. Histamine inhibits conducted vasodilation through endothelium-derived NO production in arterioles of mouse skeletal muscle. FASEB J. 18, 280–286 (2004)
Funding Information
  • National Institutes of Health (R01‐HL41026, R21‐AG19347, RO1‐HL57665, R37‐HL28373, PO1‐DK38979)