The coronary effects of parathyroid hormone

Horm Res. 2004;61(5):234-41. doi: 10.1159/000076628. Epub 2004 Feb 6.

Abstract

Objective: The aim of the present study was to characterize the role of the ATP-sensitive potassium channels (K(+)(ATP)) in the coronary dilator action of parathyroid hormone (PTH).

Methods: Dose-response curves of intracoronary administrated PTH (0.15-1.33 nmol) were obtained in control phases and during continuous intracoronary administration of the K(+)(ATP) channel-selective antagonist glibenclamide (0.1-1.0 micromol/min) in dogs (n = 13).

Results: Increments of integrated coronary conductance (excess coronary conductance) at PTH doses of 0.15 and 1.33 nmol were 1.17 versus 0.03 ml/mm Hg (p < 0.05) and 4.03 versus 0.94 ml/mm Hg (p < 0.05) in the control versus during maximal blockade, respectively.

Conclusion: The results indicate that the activation of K(+)(ATP) channels significantly contributes to the PTH-induced coronary vasodilation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / physiology
  • Animals
  • Cattle
  • Coronary Vessels / drug effects
  • Coronary Vessels / physiology*
  • Dogs
  • Dose-Response Relationship, Drug
  • Female
  • Glyburide / pharmacology
  • Male
  • Parathyroid Hormone / administration & dosage
  • Parathyroid Hormone / pharmacology
  • Parathyroid Hormone / physiology*
  • Peptide Fragments / administration & dosage
  • Peptide Fragments / pharmacology
  • Potassium Channel Blockers / pharmacology
  • Potassium Channels / physiology
  • Vasodilation / drug effects
  • Vasodilation / physiology*

Substances

  • Parathyroid Hormone
  • Peptide Fragments
  • Potassium Channel Blockers
  • Potassium Channels
  • Adenosine Triphosphate
  • Glyburide