Vasopressin autoreceptors and nitric oxide-dependent glutamate release are required for somatodendritic vasopressin release from rat magnocellular neuroendocrine cells responding to osmotic stimuli.
Magnocellular neuroendocrine cells of the supraoptic nucleus (SON) release vasopressin (VP) systemically and locally during osmotic challenge. Although both central VP and nitric oxide (NO) release appear to reduce osmotically stimulated systemic VP release, it is unknown whether they interact locally in the SON to enhance somatodendritic release of VP, a phenomenon believed to regulate systemic VP release. In this study, we examined the contribution of VP receptor subtypes and NO to local VP release from the rat SON elicited by systemic injection of 3.5 m saline. Treatment of SON punches with VP receptor antagonists decreased osmotically stimulated intranuclear VP release. Similarly, blockade of NO production, or addition of NO scavengers, reduced stimulated VP, glutamate, and aspartate release, suggesting that local NO production and activity are critical for osmotically induced intranuclear VP and excitatory amino acid release. An increase in endogenous NO release from SON punches in response to hyperosmolality was confirmed by enzymatic NO assay. Consistent with enhanced glutamate and VP release from stimulated rat SON punches, the ionotropic glutamate receptor blocker kynurenate decreased stimulated local VP release without affecting NO release. These data suggest that NO enhances local VP release in part by facilitating local release of glutamate/aspartate and that glutamate receptor activity is required for the stimulation of local VP release by osmotic challenge. Collectively, these results suggest that local VP receptors, NO, and glutamatergic signaling mediate the amplification of intranuclear VP release during hyperosmolality and may contribute to efficient, but not exhaustive, systemic release of VP during osmoregulatory challenge.
Gillard
E R
ER
Department of Cell Biology and Neuroscience, 2110 Biological Sciences Building, University of California at Riverside, Riverside, California 92521, USA. erachelgillard@yahoo.com
Coburn
C G
CG
de Leon
A
A
Snissarenko
E P
EP
Bauce
L G
LG
Pittman
Q J
QJ
Hou
B
B
Currás-Collazo
M C
MC
D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D017660:Autoreceptors / Q000378:metabolism*; D018846:Excitatory Amino Acids / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism*; D066298:In Vitro Techniques; D009490:Neurosecretory Systems / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D009569:Nitric Oxide / Q000096:biosynthesis / Q000378:metabolism*; D009995:Osmosis; D020033:Protein Isoforms / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017483:Receptors, Vasopressin / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*; D012965:Sodium Chloride / Q000494:pharmacology*; D013495:Supraoptic Nucleus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D014667:Vasopressins / Q000378:metabolism; D014882:Water-Electrolyte Balance / Q000502:physiology
D000596:Amino Acids; D017660:Autoreceptors; D018846:Excitatory Amino Acids; D020033:Protein Isoforms; D017483:Receptors, Vasopressin; D014667:Vasopressins; D009569:Nitric Oxide; D018698:Glutamic Acid; D012965:Sodium Chloride