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Related Experiment Videos

Systemic vascular autoregulation amplifies pressor responses to vasoconstrictor agents.

P J Metting1, P M Stein, B A Stoos

  • 1Department of Physiology, Medical College of Ohio, Toledo 43699.

The American Journal of Physiology
|January 1, 1989
PubMed
Summary

Systemic autoregulation amplifies pressor agent effects. Vasoconstriction from elevated mean arterial pressure (MAP) significantly boosts total peripheral resistance (TPR) responses to angiotensin II, vasopressin, and norepinephrine.

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Area of Science:

  • Cardiovascular Physiology
  • Autoregulation
  • Pharmacology

Background:

  • Pressor agents increase mean arterial pressure (MAP).
  • Systemic autoregulation influences vascular resistance.
  • The contribution of autoregulation to pressor agent effects is not fully understood.

Purpose of the Study:

  • To quantify the role of systemic autoregulation in the pressor response to intravenous angiotensin II (ANG II), arginine vasopressin (AVP), and norepinephrine (NE).
  • To differentiate between direct vasoconstrictor effects and pressure-induced autoregulatory responses.

Main Methods:

  • Experiments conducted in seven conscious dogs with blocked autonomic ganglionic transmission.
  • MAP elevation using titrated infusions of ANG II, AVP, or NE.

Related Experiment Videos

  • MAP control at either hypertensive or normotensive levels during constant pressor agent infusion.
  • Measurement of aortic pressure, central venous pressure, and cardiac output to calculate total peripheral resistance (TPR).

    • Main Results:

    • Total peripheral resistance (TPR) was higher when MAP was maintained at hypertensive levels compared to normotensive levels during pressor agent infusion.
    • Pressure-induced increases in TPR accounted for a significant portion of the total MAP increase: 74% for AVP, 62% for NE, and 34% for ANG II.
    • Autoregulatory vasoconstriction significantly amplified the pressor effects of all tested agents.

    Conclusions:

    • Systemic autoregulation plays a crucial role in amplifying the pressor effects of ANG II, AVP, and NE.
    • A substantial part of the observed increase in total peripheral resistance during pressor agent administration is a consequence of autoregulatory responses to elevated MAP.
    • Direct vasoconstrictor actions of pressor agents are significantly potentiated by secondary autoregulatory mechanisms.