Proceedings of The Physiological Society

Kings College London (2005) J Physiol 565P, C167

Communications

Different mechanisms underlie respiratory rhythms in muscle and thermoregulatory vasoconstrictor sympathetic activity

Huang, Chunhua ; Marina, Nephtali ; GILBEY, Michael P;

1. Physiology, UCL, London, United Kingdom.


The pattern and rhythm in sympathetic activity regulating many targets indicates cardiorespiratory coupling (Numao et al. 1987; Smith & Gilbey, 2000). Smith & Gilbey (2000) concluded that central respiratory drive (CRD)-related rhythms in renal nerve activity arose directly from central respiratory networks, whereas activity supplying thermoregulatory circulations (CVC) resulted from entrainment of autonomous sympathetic rhythm generators (T-rhythm: Chang et al. 1999). Here we investigate the mechanism(s) underlying cardiorespiratory interactions in sympathetic muscle vasoconstrictor (MVC) activity. S-D rats (male, 280-330g, n=6) were anaesthetised (sodium pentobarbitone 60 mg kg-1 I.P.; supplemented with 5-10 mg α-chloralose I.V., as required until humane killing with anaesthetic), vagotomised, sino-aortic denervated and pneumothorax. During positive pressure ventilation (2.0 Hz, 1.5-2.ml) CRD (index phrenic nerve (PN) activity) was adjusted by adding COnull2 to the inspired gas mixture. Arterial blood gases and pH were assessed after each data collection. A neuromuscular blocker (gallamine triethiodide 16mg kg-1 h-1; Smith & Gilbey, 2000) was administered. Autospectra were computed from rectified and smoothed (τ=20ms) population recordings from a gastrocnemius nerve (GN, MVC activity), the plantar aspect of the ipsilateral tibial nerve (TNp, activity of typical CVC activity) and PN (Huang & Gilbey, 2003). Whereas at all levels of CRD tested a dominant peak in the autospectra of MVC activity was observed at rhythmic PN discharge frequency (fPN: linear regression analysis, 21 pts, Y-intercept=0, slope=1, r2=1), a dominant peak in powerspectra of CVC activity was observed at fPN only when CRD was at an enhanced level (PnullaCOnull2 59±3): at normal levels of CRD and in central apnoea the T-rhythm dominated (linear regression analysis, 21 pts, Y-intercept=0.75, slope=-0.24, p=0.0006, r2=0.47). PN-triggered averages of MVC and CVC activities showed that during enhanced CRD both nerve activities reached a peak in early expiration, however peak MVC activity was sustained (duration 0.46±0.04 of phrenic cycle), whereas peak CVC activity subsided rapidly (duration 0.08±0.02; durations significantly different P<0.003, unpaired t test). Thus, two distinct mechanisms underlie the CRD-related MVC and CVC rhythms. We provide evidence that CRD entrains autonomous sympathetic rhythm (T-rhythm) generators associated with CVC activity. No such evidence was obtained concerning sympathetic networks controlling MVC activity.

Where applicable, experiments conform with Society ethical requirements