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This Article Full Text Full Text (PDF) All Versions of this Article: 584/3/819    most recent jphysiol.2007.134338v2 jphysiol.2007.134338v1 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 Google Scholar Google Scholar Articles by Park, J. Articles by Swain, G. M. Search for Related Content PubMed PubMed Citation Articles by Park, J. Articles by Swain, G. M. Related Collections Neuroscience

¹ Department of Chemistry and the Neuroscience Program, Michigan State University, East Lansing, MI 48824, USA
² Department of Pharmacology and Toxicology and the Neuroscience Program, Michigan State University, East Lansing, MI 48824, USA

As arteries are resistance blood vessels while veins perform a capacitance function, it might be expected that sympathetic neural control of arteries and veins would differ. The function of sympathetic nerves supplying mesenteric arteries (MA) and veins (MV) in rats was investigated using in vitro continuous amperometry with a carbon fibre microelectrode and video imaging. We simultaneously measured noradrenaline (NA) overflow at the blood vessel adventitial surface and vasoconstriction evoked by electrical stimulation of perivascular sympathetic nerves. Sympathetic nerve arrangement was studied using glyoxylic acid-induced fluorescence of NA. We found that: (i) there were significant differences between MA and MV in the arrangement of sympathetic nerves; (ii) frequency–response curves for NA overflow and vasoconstriction for MV were left-shifted compared to MA; (iii) the P2X receptor antagonist, pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 10 µM), reduced constrictions in MA but not in MV while the ₁-adrenergic receptor antagonist, prazosin (0.1 µM), blocked constrictions in MV but not in MA; (iv) NA overflow for MA was enhanced by the ₂-adrenergic receptor antagonist, yohimbine (1.0 µM), and attenuated by the ₂-adrenergic receptor agonist, UK 14,304 (1.0 µM), while yohimbine and UK 14,304 had little effect in MV; (v) cocaine (10 µM) produced larger increases in NA overflow in MA than in MV; (vi) UK 14,304 constricted MV but not MA while yohimbine reduced constrictions in MV but not MA. We conclude that there are fundamental differences in sympathetic neuroeffector mechanisms in MA and MV, which are likely to contribute to their different haemodynamic functions.

(Received 11 April 2007; accepted after revision 29 August 2007; first published online 30 August 2007)
Corresponding author G. M. Swain: Department of Chemistry and the Neuroscience Program, Michigan State University, East Lansing, MI 48824, USA. Email: swain{at}chemistry.msu.edu