Membrane electrical mechanism of basilar artery constriction and pial artery dilation by norepinephrine

D. R. Harder, Peter W. Abel, K. Hermsmeyer

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

To study the mechanism by which norepinephrine acts on vascular muscle cell membrane, the authors recorded membrane potential with intracellular microelectrodes in isolated cat basilar and pial arteries. On addition of norepinephrine concentrations less than 1 μM, pial arteries hyperpolarized and relaxed while basilar arteries depolarized and contracted. Relaxation and hyperpolarization of the pial arteries occurred without the need for addition of any other drug, which indicates the relaxation of spontaneous tone. The relaxation and hyperpolarization could be completely blocked by addition of propranolol before exposure to norepinephrine. The depolarization and contraction of both basilar and pial arteries was blocked by the previous exposure to phentolamine. Electrical spikes were not found spontaneously, but could be induced in both arteries by tetraethylammonium and subsequent addition of norepinephrine, blockable by phentolamine. The authors concluded the membrane property differences between basilar and pial arteries result in qualitatively different effects of norepinephrine.

Original languageEnglish
Pages (from-to)1237-1242
Number of pages6
JournalCirculation Research
Volume49
Issue number6
StatePublished - 1981
Externally publishedYes

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Basilar Artery
Constriction
Dilatation
Norepinephrine
Arteries
Membranes
Phentolamine
Tetraethylammonium
Microelectrodes
Propranolol
Membrane Potentials
Muscle Cells
Blood Vessels
Cats
Cell Membrane
Pharmaceutical Preparations

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Membrane electrical mechanism of basilar artery constriction and pial artery dilation by norepinephrine. / Harder, D. R.; Abel, Peter W.; Hermsmeyer, K.

In: Circulation Research, Vol. 49, No. 6, 1981, p. 1237-1242.

Research output: Contribution to journalArticle

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