Our previous studies have shown that stimulation of the anterior ventral third ventricular region increases atrial natriuretic peptide (ANP) release, whereas lesions of this structure, the median eminence, or removal of the neural lobe of the pituitary block ANP release induced by blood volume expansion (BVE). These results indicate that participation of the central nervous system is crucial in these responses, possibly through mediation by neurohypophysial hormones. In the present research we investigated the possible role of oxytocin, one of the two principal neurohypophysial hormones, in the mediation of ANP release. Oxytocin (1-10 nmol) injected i.p. caused significant, dose-dependent increases in urinary osmolality, natriuresis, and kaliuresis. A delayed antidiuretic effect was also observed. Plasma ANP concentrations increased nearly 4-fold (P < 0.01) 20 min after i.p. oxytocin (10 nmol), but there was no change in plasma ANP values in control rats. When oxytocin (1 or 10 nmol) was injected i.v., it also induced a dose-related increase in plasma ANP at 5 min (P < 0.001). BVE by intra-atrial injection of isotonic saline induced a rapid (5 min postinjection) increase in plasma oxytocin and ANP concentrations and a concomitant decrease in plasma arginine vasopressin concentration. Results were similar with hypertonic volume expansion, except that this induced a transient (5 min) increase in plasma arginine vasopressin. The findings are consistent with the hypothesis that baroreceptor activation of the central nervous system by BVE stimulates the release of oxytocin from the neurohypophysis. This oxytocin then circulates to the right atrium to induce release ofANP, which circulates to the kidney and induces natriuresis and diuresis, which restore body fluid volume to normal levels.Our previous studies have shown that the central nervous system controls atrial natriuretic peptide (ANP) release; osmotic, cholinergic, and noradrenergic stimulation of the anterior ventral third ventricular (AV3V) region induces ANP release (1). Conversely, lesions of the AV3V region decreased resting plasma ANP concentrations and largely blocked ANP release in response to blood volume expansion (BVE) (2). Neurons containing ANP, termed ANPergic neurons, have their perikarya in the AV3V region and axons that project to the median eminence and neural lobe of the pituitary gland (3-5). These appear critical to the volume expansion-induced release of ANP since antisera directed against ANP injected into the third ventricular region of rats (6) or sheep (7) can inhibit volume expansion-induced ANP release.Lesions of the median eminence or neural lobe of the pituitary gland, which interrupt neuronal pathways projecting from the AV3V region to the neurohypophysis, blocked volume expansion-induced ANP release (2). Therefore, we hypothesized that release of one or more neuropeptides from the neurohypophysis caused the increase in ANP release after volume expansion. As indicated above, the axons of ANP neurons terminate in the neuro...
Adult Wistar male rats underwent immobilization stress (IS) during forty minutes. PRL secretion presented a remarkable increase after 5 minutes, and it was higher than pre-stress values during the entire duration of the experiment. The blockade of beta-1 adrenoceptors by icv injections of practolol did not modify IS-induced PRL release. IPS 339, a selective antagonist of beta-2 adrenoceptors, also injected icv, reduced PRL secretion during stress in a dose dependent fashion. The blockade of PRL secretion due to IPS 339 was reverted by a previous icv administration of salbutamol, a classical beta-2 agonist. The data presented here suggest that central beta-2 adrenoceptors activation is an important step in the control of stress-induced PRL secretion.
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