M. Kadekaro et al., ROLE OF NO ON VASOPRESSIN AND OXYTOCIN RELEASE AND BLOOD-PRESSURE RESPONSES DURING OSMOTIC STIMULATION IN RATS, American journal of physiology. Regulatory, integrative and comparative physiology, 42(3), 1997, pp. 1024-1030
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
.