HYPOTHALAMIC OSMOREGULATION FOR VASOPRESSIN RELEASE IN STREPTOZOTOCIN-DIABETIC RATS INVIVO AND INVITRO

The central osmoregulation mechanism for vasopressin (VP) release was studied in the streptozotocin diabetic (STZ-DM) rat. Electrical activities of the VP-producing cell in the supraoptic nucleus (SON) were recorded extracellularly and compared with those in the control rat both in vivo and in vitro. Neuronal activities in the periventricular area (PVA) were also recorded in the in vitro experiment. Hyperosmolar stimulation which was done with an intraperitoneal injection of 1.0 M NaCl (4 ml/kg) resulted in an increase in plasma osmolality both of STZ-DM (increased by 14 +/- 2 mOsml/kg H2O) and control rats (15 +/- 3 mOsmol/kg H2O). Increased plasma osmolality caused significant increase in the mean discharge rate of VP-producing cells in the control animals, but only an insignificant change in STZ-DM rats. In the hypothalamic slice preparations incubated in the artificial cerebrospinal fluid (301 +/- 2 mOsml/kg H2O), VP-producing cells in control rats increased their discharge rate linearly as the osmolality (310 +/- 2 and 320 +/- 1 mOsmol/kg H2O) or concentration (10(-8) and 10(-6) M) of angiotensin II (AGII) of the perfusate was increased stepwise, but there was no change in response to either stimulus in STZ-DM rats. On the other hand, there was no difference in sensitivity to osmolality and AGII of PVA neurons in both animal groups. These data indicate that lower sensibility to osmotic change of VP-producing cells in STZ-DM rats may depend, at least partially, upon the disturbance of osmo- and AGII-sensitivity in VP-producing cells themselves, and that these changes seem to be restricted to SON VP-producing cells.