Vasopressin release during nonhypotensive hemorrhage and angiotensin II infusion

R. E. Shade, L. Share

    Research output: Contribution to journalArticle

    23 Scopus citations

    Abstract

    These experiments were designed to determine whether angiotensin II (AII) could potentiate the increase in plasma vasopressin (ADH) concentration produced by continuous, nonhypotensive hemorrhage in nephrectomized dogs. Infusion of AII (10 ng/kg/min) into a common carotid artery in nonbled dogs did not increase plasma ADH levels, suggesting that increases in carotid arterial plasma AII concentration alone do not stimulate an increase in ADH release. Subsequently, nephrectomized dogs subjected to nonhypotensive hemorrhage (0.44 ml/kg/min) were infused as follows: 0.9% saline intravenously, AII (10 ng/kg/min) intravenously, or AII (10 ng/kg/min) into the carotid. The plasma ADH concentration increased in all three groups of dogs during hemorrhage. Although the AII infused dogs demonstrated significant increases in plasma ADH levels earlier during hemorrhage, these changes were small; there were no statistically significant differences in plasma ADH concentrations among the 3 groups. These results suggest that increases in plasma AII concentration have little or no significant effect on the volume control of ADH release.

    Original languageEnglish (US)
    Pages (from-to)149-154
    Number of pages6
    JournalAmerican Journal of Physiology
    Volume228
    Issue number1
    StatePublished - Jan 1 1975

    ASJC Scopus subject areas

    • Physiology (medical)

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