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AT1 receptor blockade and the sympathoadrenal response to insulin-induced hypoglycemia in humans

R H Worck1, H Ibsen, E Frandsen

  • 1Department of Medicine C, University of Copenhagen, Denmark.

Insights

Angiotensin II's role in adrenal catecholamine release was studied during hypoglycemia. AT1 receptor blockade did not alter epinephrine or norepinephrine release, suggesting the interaction isn't mediated by AT1 receptors in humans.

Area of Science:

  • Endocrinology
  • Neuroscience
  • Cardiovascular Physiology

Background:

  • Angiotensin II facilitates adrenal catecholamine release across species.
  • The specific role of the AT1 receptor in this interaction during human hypoglycemia is not fully understood.

Purpose of the Study:

  • To investigate the effect of AT1 receptor blockade on medullary epinephrine and musculocutaneous norepinephrine release during insulin-induced hypoglycemia in humans.
  • To determine if the sympathoadrenal response to hypoglycemia is mediated via AT1 receptors.

Main Methods:

  • 16 healthy volunteers received either losartan (AT1 receptor blocker) or placebo.
  • An intravenous insulin bolus was administered to induce hypoglycemia.
  • Measurements of catecholamines, hormones, and cardiovascular parameters were taken over 150 minutes.

Main Results:

  • AT1 receptor blockade effectively increased renin and angiotensin II levels, inhibited aldosterone, and decreased mean arterial pressure.
  • Insulin-induced hypoglycemia led to a 23-fold increase in epinephrine and a 4-fold increase in norepinephrine release.
  • These sympathoadrenal responses, including heart rate and blood flow changes, were independent of AT1 receptor blockade.

Conclusions:

  • The facilitating effect of angiotensin II on adrenal catecholamine release during human hypoglycemia is not mediated by AT1 receptors.
  • This suggests an alternative pathway for angiotensin II interaction with the sympathoadrenal axis in humans.

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