ROLE OF NO ON VASOPRESSIN AND OXYTOCIN RELEASE AND BLOOD-PRESSURE RESPONSES DURING OSMOTIC STIMULATION IN RATS

N-G-nitro-L-arginine methyl ester (L-NAME, 250 mu g/5 mu l), an inhibi tor of nitric oxide (NO) synthase, or artificial cerebrospinal fluid ( 5 mu l) was administered intracerebroventricularly to conscious naive rats or to rats treated subcutaneously (15 ml/kg) with NaCl (0.15, 0.4 5, or 1.0 M) or given a needle prick only. Intracerebroventricular inj ection of L-NAME increased plasma concentration of vasopressin (TrP) a nd oxytocin (OT) in control naive rats, indicating that NO tonically i nhibits basal secretion of both hormones during isosmotic isovolemic c onditions. Osmotic stimulation with hypertonic saline (0.45 and 1.0 M NaCl) elevated plasma levels of both hormones as expected. Central blo ckade of NO synthase further enhanced secretion of OT during mild, but not strong, osmotic stimulation, whereas the high levels of VP remain ed unaffected by L-NAME. In animals treated with the needle prick or 0 .15 M NaCl, only OT levels were increased after L-NAME. Therefore, NO selectively inhibits OT release in response to a painful stimulus (nee dle prick) and moderate osmotic stimulation to promote a preferential release of VP. A transient presser response was observed after subcuta neous injection of 0.15 and 0.45 M NaCl, but a sustained response was obtained after 1.0 M NaCl. Regardless of whether the animals received NaCl solutions, however, treatment with L-NAME elevated blood pressure in all animals. Thus NO-induced vasodilation maintains basal arterial blood pressure and limits the presser response to osmotic stimulation .