PRESYNAPTIC HISTAMINE H1- AND H3-RECEPTORS MODULATE SYMPATHETIC NEUROTRANSMISSION IN ISOLATED GUINEA-PIG VASDEFERENS

The action of (R)-alpha-methylhistamine (alpha-MeHA), a selective H-3- receptor agonist, on field stimulation induced contraction of guinea p ig vas deferens was.composed of 2 components: the 'inhibition'' (0.1-1 00 nmon.L-1) and the ''enhancement'' (1-10 mumol.L-1). In the presence of histamine H-1 antagonist, chlorpheniramine (I mumol.L-1), alpha-Me HA (0.1 nmol.L-1-10 mumol. L-1) showed only a concentration-dependent inhibition. Selective histamine H-3-receptor antagonist, thioperamide (I nmol.L-1-10 mumol.L-1) antagonized the inhibitory effect of alpha-M eHA and increased the contractile amplitude of vas deferens elicited b y field pulses when thioperamide was used alone. Alpha-MeHA 10 mumol.L -1 enhanced the contractile amplitude, which was reversed by chlorphen iramine 1 mumol.L-1, but not by ranitidine (1 mumol.L-1). Pyridelethyl amine, an H-1-receptor agonist, facilitated concentration-dependently the contractile response of vas deferens. The effect was antagonized b y chlorpheniramine, but not by ranitidine. Dimaprit, an H2-receptor ag onist had no effect on the field stimulation induced sympathetic respo nse. Both alpha-MeHA and pyridelethylamine failed to influence the con traction of vas deferens elicited by direct field stimulation in smoot h muscle or by exogenously applied norepinephrine. It was concluded th at histamine H-1- and H-3-receptors existed in sympathetic terminals o f guinea pig vas deferens and facilitated or inhibited the sympathetic neurotransmission.