Related Experiment Videos
Hypothesis for the initiation of vasomotion
H Peng1, V Matchkov, A Ivarsen
1Department of Physiology and Danish Biomembrane Research Centre, Aarhus University, Aarhus, Denmark.
Circulation Research
|April 28, 2001
Summary
Vasomotion initiation involves synchronized calcium release from the sarcoplasmic reticulum (SR) in vascular smooth muscle cells. This synchronization, mediated by ion currents and membrane potential oscillations, drives arterial tone regulation.
Area of Science:
- Physiology
- Cardiovascular Research
- Cellular Biology
Background:
- Vasomotion, the rhythmic alteration of arterial tone, is crucial for blood flow regulation.
- The precise mechanisms initiating vasomotion, particularly the synchronization of cellular activity, remain incompletely understood.
Purpose of the Study:
- To propose and validate a model for the initiation of vasomotion.
- To elucidate the role of calcium (Ca2+) release synchronization in vascular smooth muscle cells.
Main Methods:
- Confocal Ca2+ imaging and isometric force measurements in rat resistance arteries.
- Patch-clamp electrophysiology and microelectrode recordings in isolated smooth muscle cells.
- Experimental manipulation using norepinephrine, endothelium, and 8-bromo-cGMP.
Main Results:
- Initially unsynchronized Ca2+ waves within vascular smooth muscle cells were observed.
- Endothelium presence or 8-bromo-cGMP induced synchronized Ca2+ oscillations and vasomotion.
- Ca2+ release activated cGMP-dependent inward currents and membrane depolarization in smooth muscle cells.
Conclusions:
- Vasomotion is initiated by synchronized Ca2+ release from the sarcoplasmic reticulum, driven by intracellular oscillators.
- Ion currents across the cell membrane, modulated by cyclic GMP (cGMP), synchronize these oscillators.
- A diffuse array of cellular oscillators, entrained by membrane potential oscillations, acts as the vascular wall pacemaker.