Evidence for the presynaptic location of the alpha-adrenoceptors which regulate noradrenaline release in the rat submaxillary gland

Summary Fifteen days after duct ligation, the wet weight of the rat submaxillary gland was reduced to 40% of the contralateral control. Under these experimental conditions, the noradrenaline (NA) content expressed as g/g was 1.2±0.1 in the control glands and 1.9±0.2 in the atrophied glands.The accumulation of ³H-NA in the tissue expressed as Ci/gland, did not differ when the atrophied glands were compared with the corresponding controls. Consequently, the uptake and retention of ³H-NA was not modified by the atrophy of the secretory cells of the gland.The spontaneous efflux of radioactivity from normal and atrophied submaxillary glands prelabelled with ³H-NA was similar. The analysis of the metabolic pattern in both experimental groups revealed that in the spontaneous outflow and also during potassium-induced depolarization, the formation of the O-methylated metabolite, ³H-normetanephrine (NMN) was reduced by more than 50% in the atrophied glands. During depolarization induced by K⁺, a 2-fold increase in the outflow of the deaminated glycol ³H-3,4-dihydroxyphenylglycol (DOPEG) was observed.The effect of phentolamine on the release of radioactivity induced by 60 mM K⁺ in normal and in atrophied submaxillary gland slices prelabelled with ³H-NA was also investigated. In both experimental groups, the fractional release of total radioactivity induced by K⁺ was similar. Phentolamine, 3.1 M, produced a 3-fold increase in the fractional release of radioactivity both in the control and the atrophied glands. These results indicate that the increase of K⁺-induced release of ³H-NA induced by phentolamine was independent of the presence or absence of the postsynaptic structures. It is concluded that phentolamine increases transmitter release by blocking alpha-adrenoceptors located in the noradrenergic nerve endings of the rat submaxillary gland.