Acetylcholine induces contraction in vertebral arteries from treated hypertensive patients

J. R. Charpie, K. D. Schreur, S. M. Papadopoulos, R. C. Webb

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

Endothelium-dependent vasodilatation to acetylcholine is abnormal in animal models of hypertension. This abnormality reflects a change in the balance of relaxing and contracting factors produced in the vascular wall. In human cerebral arteries, endothelin has been implicated in the abnormal vasoconstrictor response following subarachnoid hemorrhage. This study tests the hypothesis that cerebral arteriolar dilatation to acetylcholine is reduced in clinical hypertension due to an overproduction of endothelin. Our results show that at high concentrations of muscarinic agonist (0.3-3 μM), human vertebral arteries from hypertensive patients contract whereas those from normotensive patients remain maximally dilated. We conclude that the normal dilator response to acetylcholine is abrogated in vertebral arteries from treated hypertensive patients but endothelin-1 does not contribute to the abnormal responsiveness.

Original languageEnglish (US)
Pages (from-to)87-99
Number of pages13
JournalClinical and experimental hypertension
Volume18
Issue number1
DOIs
StatePublished - Jan 1 1996
Externally publishedYes

    Fingerprint

Keywords

  • acetylcholine
  • endothelin-1
  • hypertension
  • serotonin
  • vertebral arteries

ASJC Scopus subject areas

  • Internal Medicine
  • Physiology

Cite this