Arachidonic acid regulation of vasopressin release and intracellular Ca2+ in neurohypophysial nerve endings.
The effects of arachidonic acid (AA) and arachidonic acid metabolites on vasopressin secretion and on intracellular free calcium concentration ([Ca2+]i) from both intact and streptolysin-O permeabilized isolated nerve endings of the rat neurohypophysis were studied. Arachidonic acid induced a dose-dependent increase in resting vasopressin (AVP) secretion in both intact and streptolysin-O permeabilized nerve endings. Although AA also dose-dependently induced an increase in [Ca2+]i in intact nerve endings, the AA-induced secretory response was largely independent of an increase in [Ca2+]i. Secretory responses in intact nerve endings showed AA-induced secretion to be sustained and that AA-induced vasopressin secretion occurs via exocytosis. Arachidonic acid also dose-dependently potentiated K+-depolarization evoked vasopressin release. The potentiation of secretion occurred despite an AA-induced reduction in K+-evoked Ca2+ influx. In addition, AA reinitiated secretion following a decline in the Ca2+-dependent exocytotic secretory response suggesting a separate secretory mechanism from Ca2+-induced secretion. Inhibition of the metabolic pathways for AA suggested that AA itself mediates the secretory effects and that AA is likely subject to rapid metabolism by lipoxygenases.
Stuenkel
E L
EL
Department of Physiology, University of Michigan, Ann Arbor 48109, USA. esterm@umich.edu
Dayanithi
G
G
Nordmann
J J
JJ
D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D008297:Male; D010904:Pituitary Gland, Posterior / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014667:Vasopressins / Q000378:metabolism*
D001095:Arachidonic Acids; D014667:Vasopressins; D002118:Calcium