No abstract

SUMMARY1. The role of the Al and A2 noradrenergic cell groups of the caudal medulla in regulating the activity of paraventricular nucleus neurosecretory cells was examined with electrophysiological methods in anaesthetized male Sprague-Dawley rats.2. Antidromically identified neurosecretory cells were classified as vasopressin or oxytocin secreting on the basis of spontaneous firing patterns and responsivity to baroreceptor activation. The effect on cell firing of single pulses (25-200 ,uA) delivered to either the Al or A2 cell group areas was then examined using peri-stimulus histograms.3. Stimulation of the Al region enhanced the activity of 78 % of putative vasopressin-secreting neurones tested (n = 18), but failed to affect the activity of the majority (73 %) of putative oxytocin-secreting units (n = 15).4. A2 stimulation enhanced the firing rate of both putative vasopressin-(60 %, total n = 14) and putative oxytocin-secreting (70 %, total n = 27) neurones.5. Destruction of the paraventricular nucleus catecholamine terminal plexus by pre-treatment with the neurotoxin 6-hydroxydopamine abolished the facilitatory effects of both Al and A2 stimulation.6. These findings suggest that noradrenergic afferents of medullary origin facilitate the activity of paraventricular nucleus neurosecretory cells. The role of the projection from the Al cell group appears to differ from that of the A2 group, however, in that its effects are specific to putative vasopressin-secreting units.

It has been suggested that ACTH secretion in response to selected stimuli may be modulated by angiotensin II (AII) via direct action at the level of the corticotrope or through central actions to facilitate CRF secretion into the hypophysial-portal circulation. These hypotheses were evaluated in the present series of experiments. Our failure to observe a significant portal to peripheral plasma immunoreactive (ir) AII gradient suggested that AII does not act as a physiologically significant ACTH secretagogue at the level of the corticotrope. Central administration of synthetic AII evoked a modest dose-related stimulation of hypothalamic irCRF secretion into the portal circulation, which was reversed by the AII receptor antagonist saralasin. Activation of a known AII-positive neuronal pathway projecting from the subfornical organ (SFO) to the hypothalamic paraventricular nuclei resulted in an elevation of hypophysial-portal plasma irCRF levels and increased circulating ACTH. Pretreatment with saralasin prevented SFO stimulation-induced irCRF secretion. These observations suggest that central AII-containing pathways may participate in mediation of ACTH secretion in response to hypovolemia or hyperosmolality by facilitating irCRF secretion. Involvement of the SFO, a circumventricular organ, in this circuit is intriguing as it provides a means of monitoring peripheral irAII concentration and then converting this humoral signal into a neural signal distributed to regions regulating drinking behavior, neurohypophysial AVP secretion, and activation of the hypothalamic-pituitary-adrenal axis.