Abstract

Rat posterior pituitaries were superfused in vitro and stimulated electrically. The concentrations of vasopressin in the superfusion medium were determined by radioimmunoassay. When the pulses were applied in 10 sec trains with 10 sec intervals, vasopressin release per pulse increased progressively over the frequency range of 3-12 pulses/sec applied within the trains. The release was blocked by addition of tetrodotoxin or by removal of calcium ions from the superfusion medium. The opiate antagonist naloxone 1 or 10 microM was introduced into the superfusion medium before a second period of stimulation and enhanced vasopressin release from neurointermediate lobes after phasic stimulation at 9 pulses/sec within the trains, when compared to controls. However, naloxone 10 microM had not effect on vasopressin release from isolated neural lobes (intermediate lobes removed), although the addition of camel beta-endorphin 2 microM inhibited vasopressin release in a naloxone-reversible manner. After continuous stimulation at a frequency of 13 Hz naloxone 10 microM did not influence the release of vasopressin from neurointermediate lobes. We conclude that the evoked release of vasopressin from the neurointermediate lobe is reduced by an endogenous opiate of intermediate lobe origin, possibly beta-endorphin. Appropriate stimulation conditions are necessary for this mechanism to function.

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