TRPV1 channels contribute to hyperosmotic‐induced release of vasopressin from somata and dendrites of magnocellular neuroendocrine cells in supraoptic punches

Abstract

Magnocellular neuroendocrine cells (MNCs) in the supraoptic nucleus (SON) of the hypothalamus release the antidiuretic hormone, vasopressin (VP), in response to hyperosmotic and hypovolemic stimulation. Transient Receptor Potential Vanilloid 1 (TRPV1) receptor channels mediate osmosensitive electrical responses in MNCs and systemic VP release (Naeini et. al., 2006) but the specific mechanism linking TRPV1 channels and secretion of VP has yet to be determined. To examine the role of TRPV1 channels in somatodendritic VP release during hyperosmotic stimulation we treated acutely dissected SON punches in vitro with 350 mOsm/l Locke's solution in the presence and absence of the TRPV1 antagonist, 5‐iodoresiniferatoxin (SB366791). VP values were quantified using enzyme‐linked immunoassay. Hyperosmotic stimulation enhanced VP release and 1.5μM SB366791 attenuated this (p<0.05; n= 39). Mean (±s.e.m.) values for extracellular VP levels in isosmotic, hyperosmotic and hyperosmotic/SB366791 were 7.15±1.7, 11.1±2.8, 3.68±0.7 pg/ml μg protein, respectively. Doses of 0.15 and 10μM also reduced VP levels to 5.5±1.0 and 5.1±1.0, respectively. Immunohistochemistry showed TRPV1 immunoreactivity in SON MNCs. We conclude that TRPV1 channels in SON MNCs are activated during hyperosmotic stimulation and are required for somatodendritic VP secretion during osmotic challenge. (Supported by UC MEXUS)