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Calcium dynamics and vasomotion in rat mesenteric arteries
Alexander Schuster1, Mathieu Lamboley, Céline Grange
1Cellular Biophysics and Biomechanics Laboratory, Swiss Federal Institute of Technology, Lausanne, Switzerland. schuster@bioeng.ucsd.edu
Journal of Cardiovascular Pharmacology
|April 16, 2004
Summary
Smooth muscle cell calcium oscillations trigger vasomotion in rat mesenteric arteries. A specific intracellular calcium threshold is required, with voltage-gated calcium channels playing a key role in this vascular response.
Area of Science:
- Physiology
- Cardiovascular Biology
- Smooth Muscle Cell Biology
Background:
- Vascular smooth muscle cell (VSMC) contraction and relaxation are regulated by intracellular calcium dynamics.
- Vasomotion, the spontaneous oscillation in vascular diameter, is crucial for regulating blood flow and pressure.
- Understanding the mechanisms underlying vasomotion is essential for treating cardiovascular diseases.
Purpose of the Study:
- To investigate the relationship between smooth muscle cell calcium dynamics and arterial diameter changes during vasoconstriction and vasomotion.
- To identify the intracellular calcium threshold required to initiate vasomotion.
- To elucidate the role of specific ion channels and transporters in NE-induced vasomotion.
Main Methods:
- Measurement of smooth muscle cell calcium dynamics and diameter in intact, pressurized rat mesenteric artery segments.
- Cumulative norepinephrine (NE) concentration-response curves to induce vasoconstriction and vasomotion.
- Application of KCl depolarization to induce contraction and assess calcium thresholds.
- Pharmacological blockade of Na+/K+-ATPase and Na+/Ca2+ exchanger (NCX), and assessment of voltage-gated calcium channel involvement.
Main Results:
- A norepinephrine (NE) threshold (0.3-0.4 microM) was identified for the onset of vasomotion, linked to a critical intracellular calcium ([Ca2+]i) increase (22.2 +/- 2.6%).
- Calcium oscillations were synchronous along the vessel and phase-shifted (1.7 +/- 0.3 seconds) ahead of diameter oscillations.
- KCl-induced contraction showed a smaller [Ca2+]i threshold (9.9 +/- 4.3%), but vasomotion was still observed.
- Blockade of Na+/K+-ATPase and NCX did not abolish calcium oscillations, indicating modulatory roles, whereas voltage-gated calcium channels were crucial.
Conclusions:
- Smooth muscle cell calcium oscillations are a prerequisite for vasomotion in rat mesenteric arteries.
- A specific intracellular calcium threshold must be reached to initiate these oscillations and subsequent vasomotion.
- Voltage-gated calcium channels are critical for the vasomotion mechanism, while Na+/K+-ATPase and NCX play modulatory roles.