Role of epinephrine and norepinephrine in the metabolic response to stress hormone infusion in the conscious dog

Am J Physiol. 1997 Oct;273(4):E674-81. doi: 10.1152/ajpendo.1997.273.4.E674.

Abstract

The role of epinephrine and norepinephrine in contributing to the alterations in hepatic glucose metabolism during a 70-h stress hormone infusion (SHI) was investigated in four groups of chronically catheterized (20-h-fasted) conscious dogs. SHI increased glucagon (approximately 5-fold), epinephrine (approximately 10-fold), norepinephrine (approximately 10-fold), and cortisol (approximately 6-fold) levels. Dogs received either all the hormones (SHI; n = 5), all the hormones except epinephrine (SHI-Epi; n = 6), or all the hormones except norepinephrine (SHI-NE; n = 6). In addition, six dogs received saline only (Sal). Glucose production (Ra) and gluconeogenesis were assessed after a 70-h hormone or saline infusion with the use of tracer ([3-(3)H]glucose and [U-(14)C]alanine) and arteriovenous difference techniques. SHI increased glucose levels (108 +/- 2 vs. 189 +/- 10 mg/dl) and Ra (2.6 +/- 0.2 vs. 4.1 +/- 0.3 mg x kg(-1) x min(-1)) compared with Sal. The absence of an increase in epinephrine markedly attenuated these changes (glucose and Ra were 140 +/- 6 mg/dl and 2.7 +/- 0.4 mg x kg(-1) x min(-1), respectively). Only 25% of the blunted rise in Ra could be accounted for by an attenuation of the rise in net hepatic gluconeogenic precursor uptake (0.9 +/- 0.1, 1.5 +/- 0.1, and 1.1 +/- 0.2 mg x kg(-1) x min(-1) for Sal, SHI, and SHI-Epi, respectively). The absence of an increase in norepinephrine did not blunt the rise in arterial glucose levels, Ra, or net hepatic gluconeogenic precursor uptake (they rose to 195 +/- 21 mg/dl, 3.7 +/- 0.5 mg x kg(-1) x min(-1), and 1.7 +/- 0.2 mg x kg(-1) min(-1), respectively). In summary, during chronic SHI, the rise in epinephrine exerts potent stimulatory effects on glucose production principally by enhancing hepatic glycogenolysis, although the rise in circulating norepinephrine has minimal effects.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Blood Glucose / drug effects
  • Blood Glucose / metabolism
  • Dogs
  • Epinephrine / administration & dosage
  • Epinephrine / blood*
  • Epinephrine / pharmacology*
  • Fatty Acids, Nonesterified / blood
  • Glucagon / administration & dosage
  • Glucagon / blood
  • Glucagon / pharmacology*
  • Gluconeogenesis / drug effects*
  • Glucose / metabolism*
  • Glycerol / blood
  • Glycerol / metabolism
  • Hydrocortisone / administration & dosage
  • Hydrocortisone / blood
  • Hydrocortisone / pharmacology*
  • Infusions, Intravenous
  • Intestinal Mucosa / metabolism
  • Intestines / drug effects
  • Kidney / drug effects
  • Kidney / metabolism
  • Liver / drug effects
  • Liver / metabolism
  • Liver Circulation
  • Norepinephrine / administration & dosage
  • Norepinephrine / blood*
  • Norepinephrine / pharmacology*
  • Stress, Physiological / physiopathology*

Substances

  • Blood Glucose
  • Fatty Acids, Nonesterified
  • Glucagon
  • Glucose
  • Glycerol
  • Hydrocortisone
  • Norepinephrine
  • Epinephrine