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This Article Full Text Full Text (PDF) All Versions of this Article: 563/2/541    most recent jphysiol.2004.072900v1 Services Email this article to a friend Similar articles in this journal 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 Google Scholar Google Scholar Articles by Haug, S. J Articles by Segal, S. S Search for Related Content PubMed PubMed Citation Articles by Haug, S. J Articles by Segal, S. S

¹ The John B. Pierce Laboratory, 290 Congress Avenue, New Haven, CT 06519, USA
² Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06520, USA
³ Department of Biomedical Engineering, Yale University, New Haven, CT 06520, USA

Vasodilatation initiated on arterioles of skeletal muscle ascends into the proximal feed arteries through cell-to-cell conduction along the endothelium and into smooth muscle. Whereas perivascular sympathetic nerve activity (SNA) can inhibit conducted vasodilatation and restrict muscle blood flow, the signalling events mediating this interaction are poorly defined. Therefore, using isolated pressurized (75 mmHg) feed arteries (diameter (µm) at rest = 53 ± 3; maximum = 99 ± 2; n = 86) of the hamster retractor muscle, we tested the hypothesis that distinct yet complementary signalling pathways underlie the ability of SNA to inhibit conduction. Conducted vasodilatation was initiated using ACh microiontophoresis (1 µA; 250, 500 and 1000 ms) and SNA was initiated using local field stimulation (30–50 V; 1 ms at 2, 8 and 16 Hz). With vasodilatations of 5–20 µm, conduction increased with ACh pulse duration and was inhibited progressively as the frequency of SNA increased. During SNA, conduction was partially restored with inhibition of ₁- (0.1 µM prazosin) or ₂- (0.1 µM RX821002) adrenoreceptors and fully restored with both antagonists present. Activating ₁- (50 nM phenylephrine) or ₂- (1 µM UK 14,304) adrenoreceptors inhibited conduction partially and their simultaneous activation inhibited conduction cumulatively (P < 0.05). Elevated [K⁺]_o (30 or 40 mM) or phorbol esters (0.5 µM) also inhibited conduction yet similar constriction with L-NNA (50 µM) or Bay K 8644 (10 nM) did not. Thus, the activation of ₁- and ₂-adrenoreceptors inhibits conducted vasodilatation through complementary signalling events. With robust coupling along the endothelium, our modelling predicts that the inhibition of conduction by SNA can be explained by reduced electrical coupling through myoendothelial gap junctions or greater current leak across smooth muscle cell membranes.

(Received 29 July 2004; accepted after revision 29 November 2004; first published online 2 December 2004)
Correspondence S. S. Segal: The John B. Pierce Laboratory, Yale University School of Medicine, 290 Congress Avenue, New Haven, CT 06519, USA. Email: sssegal{at}jbpierce.org

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