AJP - Endocrinology and Metabolism, Vol 257, Issue 4 E611-E616, Copyright © 1989 by American Physiological Society
Responses of vasopressin, atrial natriuretic peptide, and blood pressure to central osmotic stimulation
K. Iitake, T. Kimura, K. Ota, M. Shoji, M. Inoue, M. Ohta, K. Sato, T. Yamamoto, M. Yasujima, K. Abe and al. et
Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
To assess whether intracerebroventricular osmoreceptors are involved in
vasopressin (AVP) and atrial natriuretic peptide (ANP) release and in the
pressor response to centrally administered hypertonic NaCl, artificial
cerebrospinal fluid (ACSF) or ACSF made hypertonic by adding 0.2 M NaCl,
0.4 M mannitol, and 0.4 M glucose in isotonic ACSF or 0.4 M urea was
infused into the 3rd ventricle of conscious rats. In addition, intravenous
infusion of [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic
acid),2-(O-methyl)tyrosine]AVP (TMeAVP), a V1-AVP antagonist, was given in
rats receiving intracerebroventricular infusion of 0.2 M NaCl in isotonic
ACSF. Intracerebroventricular 0.2 M NaCl, 0.4 M mannitol, and 0.4 M glucose
in isotonic ACSF increased plasma AVP and mean arterial pressure (MAP)
without changing heart rate (HR) or plasma ANP. Urea at 0.4 M decreased
plasma AVP and ANP with a slight rise in MAP but no change in HR. ACSF
alone did not affect plasma AVP, ANP, MAP, or HR. Intravenous TMeAVP
attenuated the pressor response to infusion of 0.2 M NaCl in isotonic ACSF,
decreased plasma ANP, but did not affect HR. These results indicate that
central osmoreceptors are involved in the release of AVP and in the pressor
response to centrally administered hypertonic NaCl.
