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Related Experiment Videos

Epinephrine synthesis by rat arteries.

B Kennedy1, H Elayan, M G Ziegler

  • 1Department of Medicine, University of California San Diego Medical Center 92103.

American Journal of Hypertension
|January 1, 1991
PubMed
Summary

Arteries synthesize epinephrine (E) from norepinephrine (NE) using an extraneuronal enzyme, distinct from adrenal phenylethanolamine N-methyltransferase (PNMT). This arterial N-methylating activity is enhanced by glucocorticoids and catecholamine depletion.

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Area of Science:

  • Biochemistry
  • Pharmacology
  • Cardiovascular Science

Background:

  • Epinephrine (E) is primarily synthesized in the adrenal medulla.
  • The enzyme phenylethanolamine N-methyltransferase (PNMT) is crucial for E synthesis.
  • Extraneuronal synthesis of E in arteries has been hypothesized but not fully elucidated.

Purpose of the Study:

  • To investigate the synthesis of epinephrine (E) in arterial tissues.
  • To characterize the enzyme responsible for N-methylation in arteries.
  • To compare arterial N-methylating activity with adrenal PNMT.

Main Methods:

  • Incubation of carotid artery and aorta homogenates with S-adenosylmethionine.
  • Assay of N-methylating activity using norepinephrine (NE) and dopamine (DA) as substrates.
  • Inhibition studies using SKF 29661, a PNMT inhibitor.
  • Assessment of arterial E levels in vivo following adrenal demedullation and catecholamine depletion.

Main Results:

  • Carotid artery and aorta homogenates synthesized epinephrine (E) from norepinephrine (NE).
  • Arterial N-methylating activity was enhanced by dexamethasone and catecholamine depletion (6-hydroxydopamine, reserpine).
  • Adrenal demedullation did not affect in vitro arterial E synthesis, suggesting extraneuronal production.

Conclusions:

  • Arteries synthesize epinephrine in vitro and likely in vivo via an extraneuronal N-methyltransferase.
  • This arterial enzyme differs from adrenal PNMT in substrate and inhibitor specificity.
  • Arterial N-methylating activity is regulated by glucocorticoids and catecholamine levels.

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