Frequency-dependence of 3H-noradrenaline secretion from human vasoconstrictor nerves: modification by factors interfering with alpha-or beta-adrenoceptor or prostaglandin E2 mediated control.

Isolated superfused field stimulated human omental arteries and veins, preincubated with 3H (-)-noradrenaline (NA) were used to study the frequency dependence of NA secretion and of the mechanisms for its local feedback control. 3H-NA secretion per shock was found to be basically a simple hyperbolic function of the stimulation frequency from 1 to 30 Hz, as long as secretion was restricted by prostaglandin E2 (PGE2). In the absence of restriction, or during facilitation, 3H-NA secretion per shock reached its maximum at 10 Hz and then declined at 30 Hz, indicating 'overload' in some link in the secretory mechanism. 3H-NA secretion was depressed by exogenous NA and by PGE2, and enchanced by isoprenaline, phentolamine and by blockade of PGE2 formation. Most of these effects were inversely related to the stimulation frequency. Attempts were made to study interactions between the different control mechanisms and to evaluate possible in vivo consequences of disturbance of adrenergic neuroeffector transmission by interference with the local control of the secretory mechanisms.