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This Article Full Text Full Text (PDF) All Versions of this Article: 570/3/637    most recent jphysiol.2005.100040v1 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 Lambert, E. Articles by Lambert, G. Search for Related Content PubMed PubMed Citation Articles by Lambert, E. Articles by Lambert, G. Related Collections Integrative

¹ Human Neurotransmitter Laboratory, Baker Heart Research Institute, Melbourne, Victoria, Australia
² School of Primary Care and Department of General Practice, Monash University, Melbourne, Victoria, Australia
³ Alfred Psychiatric Research Centre, Department of Psychological Medicine, Monash University, Melbourne, Victoria, Australia
⁴ Department of Medicine, Monash University, Alfred Hospital CECS, Melbourne, Victoria, Australia

Patients with panic disorder are at increased cardiac risk. While the mechanisms responsible remain unknown, activation of the sympathetic nervous system may be implicated. Using isotope dilution methodology, investigations of whole-body and regional sympathetic nervous activity have failed to show any differences between patients with panic disorder and healthy subjects. Using direct recording of single unit efferent sympathetic vasoconstrictor nerve activity by microneurography we examined sympathetic nervous function in patients with panic disorder more precisely than previously reported. The activity of multiunit and single unit vasoconstrictor sympathetic nerves was recorded at rest at the level of the peroneal nerve in 10 patients diagnosed with panic disorder and in nine matched healthy volunteers. Multiunit sympathetic activity was not different between the two groups (26 ± 3 bursts min^–1 in patients with panic disorder and 28 ± 3 bursts min^–1 in controls). The firing frequency of single unit vasoconstrictor neurones was also similar between the two groups (0.38 ± 0.09 versus 0.22 ± 0.03 Hz). However, the probability of firing during a sympathetic burst was higher in patients with panic disorder compared with healthy controls (45 ± 5%versus 32 ± 3%, P < 0.05). When only the neural bursts during which the vasoconstrictor neurone was active were considered, we found that in patients with panic disorder the neurones tended to fire more often in a ‘multiple spike’ pattern than in the controls (i.e. the probability of the neurone firing twice was 25 ± 3% in patients with panic disorder compared with 14 ± 3% in controls). Quantification from single vasoconstrictor unit recording provides evidence of a disturbed sympathetic firing pattern in patients with panic disorder.

(Received 12 October 2005; accepted after revision 23 November 2005; first published online 24 November 2005)
Corresponding author E. Lambert: Baker Heart Research Institute, PO Box 6492 St Kilda Road Central, Melbourne, Victoria, Australia. Email: elisabeth.lambert{at}baker.edu.au

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