The maintenance of the cell volume within physiological limits under anisosmotic conditions is an important prerequisite for survival and functioning of the cell. Cell volume alterations are also involved in numerous cellular events and are recently considered to be integrated into a physiological signal transduction network. Cell swelling induced by anisosmotic environment, hormones, oxidative stress, or substrate uptake evokes an immediate secretory burst of the material (peptide hormones, enzymes) stored in secretory vesicles from various types of the cells (endocrine cells, neurons, leukocytes, exocrine pancreatic cells). The dynamics of this secretion are indistinguishable from those induced by specific secretagogues. This regulated secretion does not require a rise in the intracellular [<$E roman Ca sup 2+>]. Using various tissues (pituitary, pancreatic islets, brain structures), hormones (prolactin, insulin, thyrotropin-releasing hormone - TRH, oxytocin), and inhibitors, we found that hormone secretion induced by cell swelling is not depressed by inhibition of stretch-activated channels (GdC13), mercury-sensitive aquaporins, protein kinase С (bisindolylmaleimide), microtubules and microfilaments (colchicine, cytochalasin) and does not involve arachidonic acid metabolites, prostaglandins, and leukotriens (indomethacin, NDGA). The blockade of <$E roman {Na sup + -K} sup +>-dependent ATPase, that of <$E roman Na sup +> channels, or that of <$E roman K sup +> channels exerted no effect on hyposmolarity-induced hormone secretion in pituitary cells. Norepinephrine, a physiological inhibitor of secretion of insulin, did not inhibit

hypotonicity-induced secretion from pancreatic islets. The participation of such a general biophysical phenomenon in physiological reactions rises a question of its specificity. Cell swelling induced by an isosmotic ethanol-containing medium evoked release of TRH from hypothalamic paraventricular nucleus and posterior pituitary, while oxytocin release (known to be engaged in the water and salt regulation) was not stimulated.

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