348 B. Szabo and E. Schlicker
Fig.5A,B.Cannabinoidsinhibit sympathetic andparasympathetic neuroeffectortransmissioninthe heart.A
Cardiac sympathetic nerves in pithed rabbits were stimulated at a frequency of 1 Hz for 30 s. Solvent (SOL)and
WIN55212-2 (WIN) were administered i.v. as indicated by thearrows. One of the WIN groups (YOH+WIN)was
pretreatedwiththeα 2 -adrenoceptorantagonistyohimbine(0.5mg/kg–1;i.v.)att= –14min.Cardioaccelerator
responses are given as percentages of the initial reference value (PRE). WIN inhibited the cardioaccelerator
response more strongly in the presence of YOH, probably because YOH prevented concurrent inhibition by
endogenous noradrenaline.BThe right vagus nerve was stimulated at a frequency of 10 Hz for 5 s. SOL, WIN
and CP55940 (CP) were administered i.v. as indicated by thearrows. Cardiodecelerator responses are given
as percentages of the initial reference value PRE.*, Significant difference from SOL (p<0.05). See Szabo et al.
(2001) for details of the experiments
a stimulatory effect mediated via vanilloid receptors (TRPV1, transient receptor
potential V1 channel) at high concentrations (Zygmunt et al. 1999; Tognetto et al.
2001; Ahluwalia et al. 2003; Nemeth et al. 2003).
The effect of cannabinoids on peripheral autonomic transmission has been
extensively reviewed by Ralevic (2003).