Foot shock stress-induced release of vasopressin in adenohypophysectomized and hypophysectomized rats.

The effect of inescapable electric foot shock stress on vasopressin (VP) release was studied in conscious rats. In sham-operated animals, foot shock stress markedly increased plasma beta-endorphin-like immunoreactivity whereas plasma VP levels (RIA) remained unchanged. However, after selective ablation of the anterior lobe of the hypophysis, foot shock stress produced an 8-fold increase in plasma VP concentrations. Injection of hypertonic saline did not change plasma VP levels in adenohypophysectomized (Ahx) rats, while in sham-operated rats VP levels increased in response to this osmotic challenge. Neurointermediate lobes or medial basal hypothalami (MBH; containing the median eminence region) were superfused in vitro and stimulated electrically; as compared to sham operations, the evoked release of VP from the neurointermediate lobes was abolished, whereas that from the MBH was markedly (13-fold) enhanced when the tissues were taken from Ahx rats. The VP-like immunoreactivity released from the MBH of Ahx rats comigrated with synthetic arginine-VP on Sephadex G-15 column chromatography. Similarly, as found in Ahx rats, foot shock stress markedly raised plasma VP levels in totally hypophysectomized rats, whereas after selective ablation of the neurointermediate lobe of the hypophysis VP levels increased only slightly after stress. In conclusion, our data indicate that 1) foot shock stress induces the release of VP from some site other than the neurohypophysis, probably from the median eminence region, in Ahx rats; and 2) an increase in plasma osmolality is a powerful stimulus for the release of VP from the neurohypophysis but cannot release VP from the median eminence region. Thus, our results support the concept of a morphological and functional differentiation of the vasopressinergic neurosecretory system.