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Pressor hyperresponsiveness in saline-infused rabbits.

T Sakamaki, J A Johnson, D W Zeigler

    Hypertension (Dallas, Tex. : 1979)
    |July 1, 1984
    PubMed
    Summary

    Saline infusion in rabbits enhances blood pressure responses to norepinephrine, indicating fluid expansion causes vascular hyperresponsiveness. A circulating factor, potentially natriuretic hormone, mediates this effect, not angiotensin II.

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    Area of Science:

    • Cardiovascular Physiology
    • Renal Physiology

    Background:

    • Expansion of body fluid volume is known to affect cardiovascular regulation.
    • The role of specific hormones in mediating pressor responses during fluid expansion requires further investigation.

    Purpose of the Study:

    • To investigate the pressor and vascular hyperresponsiveness to norepinephrine (NE) following isotonic saline infusion in conscious rabbits.
    • To determine the involvement of angiotensin II (ANG II) and other circulating factors in this hyperresponsiveness.

    Main Methods:

    • Conscious rabbits received intravenous isotonic saline infusion for 24 hours.
    • Pressor responses to NE were measured before and after saline infusion.
    • Cross-circulation experiments were performed between saline-infused and normal rabbits.

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  • Cardiac output (CO) and total peripheral resistance (TPR) were measured.

    • Main Results:

    • Saline-infused rabbits exhibited exaggerated pressor responses and increased TPR to NE compared to controls.
    • Angiotensin II (ANG II) antagonism did not attenuate the heightened pressor response.
    • Cross-circulation from saline-infused donors to normal recipients induced NE hyperresponsiveness in recipients.
    • Saline infusion increased CO and decreased TPR, but NE infusion did not alter CO, only increasing mean arterial pressure (MAP) and TPR more post-infusion.

    Conclusions:

    • Expansion of body fluid volume via saline infusion induces pressor and vascular hyperresponsiveness to NE in rabbits.
    • This hyperresponsiveness is mediated by a circulating factor, not angiotensin II.
    • Natriuretic hormone is a potential mediator of this pressor hyperresponsiveness in saline-expanded animals.