The effect of swelling on TRH and oxytocin secretion from hypothalamic structures.
1. Cell swelling induces exocytosis of material stored in secretory vesicles resulting in a secretory burst of peptidic hormones or enzymes from various types of cells including endocrine cells and neurons. We have previously shown that swelling-induced exocytosis possesses limited selectivity; hypotonic medium evokes TRH but not oxytocin release from hypothalamic paraventricular nucleus (PVN) and neurohypophysis (NH). 2. It is the aim of this study to ascertain whether the swelling-induced oxytocin secretion could be unmasked by the inhibition of specific osmotic response using Ca(2+)-free medium and GdCl(3), an inhibitor of stretch activated channels. 3. Oxytocin release from the PVN was stimulated by the hypotonic medium only in the presence of 50 or 100 microM GdCl(3.) Oxytocin release from supraoptic nucleus (SON) was also stimulated by the Ca(2+)-free hypotonic medium in the presence of GdCl(3). Oxytocin secretion from the NH was not stimulated even in the presence of GdCl(3), both in Ca(2+) containing and Ca(2+)-free medium. TRH response to swelling-inducing stimulus was not affected by the presence of GdCl(3). 4. An intranuclear oxytocin secretion to hyposmotic stimulation within the PVN and the SON could be unmasked by the inhibiting specific response by GdCl(3). At these conditions general secretory response to swelling-inducing stimuli emerged. Secretion of oxytocin from the NH was not affected by any of these treatments. 5. Peptides and proteins released after cell swelling can play an important role in the pathophysiology of ischemia and could be mediators of local or remote preconditioning. Disruption of mechanosensitive gating in magnocellular neurosecretory cells could result in an inadequate secretory response (e.g. stimulation instead of inhibition and vice versa) of hormones engaged in water and salt metabolism regulation.