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Related Experiment Videos

Homologous upregulation of human arterial alpha-adrenergic responses by guanadrel

R V Hogikyan1, M A Supiano

  • 1Department of Internal Medicine, University of Michigan, Ann Arbor.

The Journal of Clinical Investigation
|April 1, 1993
PubMed
Summary

Reduced sympathetic nervous system (SNS) activity in humans leads to homologous upregulation of arterial alpha-adrenergic responsiveness. This enhances the body's response to norepinephrine when SNS activity is suppressed.

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Area of Science:

  • Cardiovascular Physiology
  • Autonomic Nervous System Regulation
  • Pharmacology

Background:

  • The sympathetic nervous system (SNS) plays a crucial role in regulating cardiovascular function, including arterial tone.
  • Understanding how arterial adrenergic responsiveness adapts to changes in SNS activity is vital for comprehending cardiovascular homeostasis.

Purpose of the Study:

  • To investigate the hypothesis of homologous upregulation of arterial alpha-adrenergic responsiveness during suppressed sympathetic nervous system (SNS) activity in humans.
  • To determine if the arterial response to norepinephrine (NE) increases when SNS activity is reduced.

Main Methods:

  • Ten healthy young subjects were studied under placebo conditions and after SNS suppression using guanadrel.
  • Forearm blood flow (FABF) responses to intra-arterial infusions of norepinephrine, angiotensin II, and phentolamine were measured using plethysmography.

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  • Plasma norepinephrine levels and norepinephrine release rates were assessed to confirm SNS suppression.

    • Main Results:

    • Guanadrel administration successfully suppressed SNS activity, evidenced by lower plasma NE levels and reduced NE release rates.
    • Arterial alpha-adrenergic responsiveness, specifically the forearm blood flow response to norepinephrine, was significantly increased during guanadrel treatment.
    • The forearm blood flow response to angiotensin II remained unchanged, supporting the homologous nature of the observed upregulation to norepinephrine.

    Conclusions:

    • Suppression of sympathetic nervous system activity in humans induces a homologous upregulation of arterial alpha-adrenergic responsiveness.
    • This adaptive mechanism enhances the sensitivity to endogenous and exogenous norepinephrine, contributing to the maintenance of arterial tone.
    • The findings provide insights into the dynamic regulation of vascular adrenergic receptors in response to altered autonomic input.