AJP - Regulatory, Integrative and Comparative Physiology, Vol 273, Issue 3 1024-R1030, Copyright © 1997 by American Physiological Society

ARTICLES

Role of NO on vasopressin and oxytocin release and blood pressure responses during osmotic stimulation in rats

M. Kadekaro, H. Liu, M. L. Terrell, S. Gestl, V. Bui and J. Y. Summy-Long
Division of Neurosurgery, University of Texas Medical Branch at Galveston, 77555-0517, USA.

NG-nitro-L-arginine methyl ester (L-NAME, 250 micrograms/5 microliters), an inhibitor of nitric oxide (NO) synthase, or artificial cerebrospinal fluid (5 microliters) was administered intracerebroventricularly to conscious naive rats or to rats treated subcutaneously (15 microliters/kg) with NaCl (0.15, 0.45, or 1.0 M) or given a needle prick only. Intracerebroventricular injection of L-NAME increased plasma concentration of vasopressin (VP) and oxytocin (OT) in control naive rats, indicating that NO tonically inhibits basal secretion of both hormones during isosmotic isovolemic conditions. Osmotic stimulation with hypertonic saline (0.45 and 1.0 M NaCl) elevated plasma levels of both hormones as expected. Central blockade of NO synthase further enhanced secretion of OT during mild, but not strong, osmotic stimulation, whereas the high levels of VP remained 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 (needle prick) and moderate osmotic stimulation to promote a preferential release of VP. A transient pressor response was observed after subcutaneous 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 pressor response to osmotic stimulation.

This article has been cited by other articles:

				J. ANTUNES-RODRIGUES, M. DE CASTRO, L. L. K. ELIAS, M. M. VALENCA, and S. M. McCANN Neuroendocrine Control of Body Fluid Metabolism Physiol Rev, January 1, 2004; 84(1): 169 - 208. [Abstract] [Full Text] [PDF]

				M. A. El-Haddad, C. R. Chao, S.-X. Ma, and M. G. Ross Neuronal NO modulates spontaneous and ANG II-stimulated fetal swallowing behavior in the near-term ovine fetus Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2002; 282(5): R1521 - R1527. [Abstract] [Full Text] [PDF]

				J. E. Stern and M. Ludwig NO inhibits supraoptic oxytocin and vasopressin neurons via activation of GABAergic synaptic inputs Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2001; 280(6): R1815 - R1822. [Abstract] [Full Text] [PDF]

				S. Lee, C. K. Kim, and C. Rivier Nitric Oxide Stimulates ACTH Secretion and the Transcription of the Genes Encoding for NGFI-B, Corticotropin-Releasing Factor, Corticotropin-Releasing Factor Receptor Type 1, and Vasopressin in the Hypothalamus of the Intact Rat J. Neurosci., September 1, 1999; 19(17): 7640 - 7647. [Abstract] [Full Text] [PDF]

				A. A. Steiner, E. C. Carnio, J. Antunes-Rodrigues, and L. G. S. Branco Role of nitric oxide in systemic vasopressin-induced hypothermia Am J Physiol Regulatory Integrative Comp Physiol, October 1, 1998; 275(4): R937 - R941. [Abstract] [Full Text] [PDF]

				M. Kadekaro, M. L. Terrell, H. Liu, S. Gestl, V. Bui, and J. Y. Summy-Long Effects of L-NAME on cerebral metabolic, vasopressin, oxytocin, and blood pressure responses in hemorrhaged rats Am J Physiol Regulatory Integrative Comp Physiol, April 1, 1998; 274(4): R1070 - R1077. [Abstract] [Full Text] [PDF]