Reduced osmoresponsiveness in magnocellular neuroendocrine neurones during chronic salt‐loading

Here, we studied the effects of salt-loading in rats on the electrophysiological behaviour of neurones that secrete oxytocin and vasopressin. After 7 days of salt-loading, the basal firing rate of both vasopressin cells and oxytocin cells in urethane-anaesthetized rats was increased by less than 1 spike s^-1, which is much less than expected from the hyperosmolality induced by saltloading. The neuronal responsiveness to acute osmotic stimuli was also markedly impaired, with no change in their responses to non-osmotic stimuli. We then undertook a systematic search of the literature for studies in salt-loaded rats that had measured oxytocin or vasopressin secretion, plasma osmolality, haematocrit or pituitary hormone content, and reviewed them in light of our electrophysiological findings. The prevailing understanding is that salt loading induces plastic changes in neuronal behaviour to promote exaggerated vasopressin secretion, but the conclusions that we draw from our electrophysiological findings in urethane-anaesthetized rats and the literature review suggest the converse - that vasopressin neurones selectively habituate to osmotic stimuli, presumably to conserve diminished pituitary stores of vasopressin while sustaining enough secretion for maximal renal effects. KEY POINTS: Seven days of 'salt-loading' produces a large increase in plasma osmolality and depletes the pituitary content of vasopressin and oxytocin, apparently reflecting enhanced secretion. Using in vivo electrophysiological recordings in urethane-anaesthetized rats, we show that, after 7 days of salt loading, the basal firing rate of both vasopressin and oxytocin cells was increased to a much lesser extent than expected from the hyperosmolality induced by acute osmotic stimuli. The neuronal responsiveness to acute osmotic stimuli was also markedly impaired with no change in their responses to non-osmotic stimuli. Our results show that these neurones strongly and selectively habituate to chronic osmotic stimuli, presumably to conserve diminished pituitary stores of hormone. Our conclusions contradict the prevailing understanding that salt loading promotes an exaggerated hyperexcitability of the hypothalamo-neurohypophysial system.