DYSFUNCTION OF PURINERGIC REGULATION OF SYMPATHETIC NEUROTRANSMISSION IN SHR/NDMCR-CP (SHR-CP) RAT

Abstract

1. The effect of 2-chloroadenosine (2CA), a P1 receptor agonist and beta,gamma-methylene ATP (betagamma mATP), a P2 receptor agonist, on the overflow of endogenous noradrenaline (NE) and the contractile response were examined in the electrically field-stimulated (EFS) (1 Hz) caudal artery obtained from Wistar-Kyoto (WKY) and SHR/NDmcr-cp (SHR-cp) rats. 2. Both 2CA and betagamma mATP reduced the EFS-evoked release of NE from the arteries of WKY. Also, 2CA significantly reduced the EFS-evoked contractile response in WKY, while it had no effect at all in SHR-cp. Betagamma mATP significantly reduced the EFS-evoked contractile response in both WKY and SHR-cp. Both 2CA and betagamma mATP did not affect the contractile response induced by NE at 1 micromol/L. 3. These results indicate that in the caudal arteries of SHR-cp, the P2 agonist but not the P1 agonist is functional in the prejunctional inhibitory regulation of adrenergic neurotransmission. This P1 dysfunction may play a role in the sympathetic hyperinnervation in metabolic syndrome.