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Endocrinology, Vol 114, 1426-1432, Copyright © 1984 by Endocrine Society
ARTICLES |
T Kimura, M Shoji, K Iitake, K Ota, K Matsui and K Yoshinaga
In order to investigate the role of central alpha 1- and alpha 2- adrenoceptors in the control of vasopressin (ADH) release and the cardiovascular system, norepinephrine (NE) (1.4 microgram/kg), methoxamine (1.4 microgram/kg), yohimbine (60 micrograms/kg), and prazosin (40 micrograms/kg) were administered via the cerebral ventricles in urethane-chloralose-anesthetized dogs after morphine sedation (n = 42). In the control study 0.9% saline was administered. NE resulted in a significant fall in blood pressure, heart rate, and ADH release. Methoxamine tended to activate the cardiovascular system, but did not affect the release of ADH significantly. Prazosin decreased blood pressure significantly with a significant rise in heart rate and ADH release. Pretreatment with prazosin did not block significantly the effect of NE on blood pressure, heart rate, and ADH release. Yohimbine did not affect the cardiovascular system and ADH release significantly. Pretreatment with yohimbine completely blocked the effect of NE on ADH release, and brought about a slight rise in blood pressure and heart rate. In none of the experiments could changes in ADH release be attributed to changes in plasma osmolality. These results indicate that central alpha 1-adrenoceptors might act to activate the cardiovascular system, but have no effects on ADH release in anesthetized dogs. On the other hand, central alpha 2-adrenoceptors might act to reduce ADH release and to depress the cardiovascular system.
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