Abstract
Guinea-pig isolated vas deferens, in which the neuronal transmitter stores were labelled by preincubation with [ 3H](−)-noradrenaline was used to study ionic mechanisms of α-autoinhibition of the secretion of [ 3H]noradrenaline evoked by transmural electrical stimulation or by depolarizing concentrations of K +. Replacement of Na + in the medium markedly enhanced K +-evoked secretion, and thus probably improved depolarization-secretion coupling. It had a dual effect on the tetrodotoxinsensitive electrically-evoked secretion: at sufficiently low Na + levels the secretory response was severely depressed, presumably because of failure of impulses to invade the varicosities. At intermediate Na + concentrations the secretory response was greater than at normal Na + levels. It is concluded that extracellular Na + depresses depolarization-secretion coupling in invaded varicosities. The depressing effect of extracellular Na + did not appear to be due to lowering of the affinity of the secretory mechanism for external Ca 2+. The inhibitory effect of exogenous or endogenous noradrenaline, or of prostaglandin E 2, on electrically or K +-evoked secretion, was reduced or abolished at low concentrations of Na +. It is suggested that the α-adrenoceptor mediated inhibition of depolarization-secretion coupling might involve the same mechanism by which extracellular sodium ions inhibit the secretion of noradrenaline.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
