Effects of ion gradients on the release of neurotransmitter from autonomic nerve endings in vivo.

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1) To investigate the effect of hypoxia on endogenous norepinephrine (NE) release from cardiac sympathetic nerve ending, we administered sodium cyanide (NaCN) for 30 min into the myocardial interstitial space through a dialysis probe and measured dialysate NE levels. During the NaCN perfusion, a marked and concentration-dependent increase in dialysate NE was observed. This cyanide induced NE response was suppressed by pretreatment with despiramine (a membranous NE transport inhibitor). Further, the cyanide induced NE response was suppressed by pretreatment with TMB-8 (intracellular Ca^<2+> antagonist) but unaffected by ω-conotoxin GVIA (NE releasing inhibitor). Our data suggest that two independent (desipramine or TMB-8 suppressive) mechanisms contributed to the amount of NE efflux induced by cyanide in in vivo cardiac sympathetic nerve.2) Acute myocardial ischemia induced by coronary occlusion increased myocardial interstitial acetylcholine (ACh) and NE levels in ischemic region, whereas, in non-ischemic region, coronary occlusion increased myocardial ACh level but decreased the NE level. The ACh release in the ischemic region is mainly attributed to local release mechanism, whereas the ACh release in the non-ischemic region depends on the increased vagal efferent nerve activity. The local release mechanism would depend on intracellular Ca^<2+> mobilization but not on N-type Ca^<2+> channel opening.