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Electrical activity underlying rhythmic contraction in human pial arteries

N I Gokina1, R D Bevan, C L Walters

  • 1A.A. Bogomoletz Institute of Physiology, Ukrainian Academy of Sciences, Kiev, Ukraine.

Circulation Research
|January 1, 1996
PubMed
Summary

Human pial arteries exhibit spontaneous contractions linked to electrical activity in smooth muscle cells. These contractions involve action potentials and depend on calcium channel activation, suggesting a role in regulating blood flow.

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Area of Science:

  • Cardiovascular Physiology
  • Neuroscience
  • Smooth Muscle Electrophysiology

Background:

  • Human pial arteries often display spontaneous, rhythmic contractions.
  • The underlying mechanisms linking electrical activity of smooth muscle cells (SMCs) to these contractions require elucidation.

Purpose of the Study:

  • To investigate the relationship between SMC electrical activity and spontaneous contractions in human pial arteries.
  • To identify the ion channels and signaling pathways involved in these vascular events.

Main Methods:

  • Simultaneous measurement of membrane potential and vessel wall force in human pial artery segments.
  • Electrophysiological recordings and pharmacological interventions (tetrodotoxin, calcium removal, nifedipine, K+ depolarization).

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Main Results:

  • Spontaneous contractions in 26/53 arterial segments correlated with periodic SMC depolarization and action potential (AP) generation.
  • SMCs in spontaneously active arteries had a resting membrane potential of -44.0 mV, differing from inactive arteries (-53.5 mV).
  • Calcium removal and nifedipine (a dihydropyridine blocker) abolished spontaneous APs and contractions, while tetrodotoxin had no effect.

Conclusions:

  • Periodic spontaneous depolarization and AP generation are the basis for spontaneous contractions in human pial arteries.
  • Dihydropyridine-sensitive, voltage-dependent calcium channels are crucial for both APs and associated contractions.
  • AP generation is proposed as a key mechanism for vasomotion in human pial arteries in vivo.