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Published on: September 22, 2011
Remifentanil induces L-type Ca2+ channel inhibition in human mesenteric arterial smooth muscle cells
Zhao-Yang Hu1, Peng-Tao Lin, Jin Liu
1Department of Pharmacology, West China Hospital, Sichuan University, 610041, Chengdu, P.R. China.
Purpose:
Remifentanil is known to cause vasodilation at standard anesthetic concentrations. The intracellular mechanisms underlying its vasodilator action may involve the activation of ion channels. The purpose of this study was to examine whether remifentanil inhibits L-type calcium channels (Ca.(L)) and provides dose-dependent effects on L-type calcium channel Ba(2+) currents (I(Ba.L)) in human mesenteric arterial smooth muscle cells.
Methods:
Using the whole-cell patch-clamp method, an in depth analysis of the mechanism of the I(Ba.L) induced by remifentanil was performed in cells which were enzymatically isolated from human mesenteric arterial smooth muscle. Ten millimolars Ba(2+) was used to replace 1.5 mM Ca(2+) to increase the amplitude of the inward current through Ca(2+)channels. L-type calcium channel Ba(2+) was elicited during 50 msec depolarizing test pulses (150 msec duration) to +80 mV (10 mV increments) from a holding potential of -60 mV. The effects of remifentanil on Ca.(L) were observed at the following concentrations: 1.21, 4.84, and 19.4 nmol.L(-1) and were compared with control.
Results:
Remifentanil produced a concentration-dependent block of I(Ba,L) with IC(50) values of 38.90 +/- 3.96 x 10(-3) micromol.L(-1). The L-type calcium channel blocker, nifedipine, antagonized these remifentanil-induced currents. Remifentanil, at all concentrations, shifted the maximum of the current-voltage relationship in the hyperpolarizing direction of I(Ba.L).
Conclusion:
Remifentanil significantly inhibits Ca.(L) channels in a concentration-dependent manner in human mesenteric arteriolar smooth muscle cells.
Insights
Remifentanil, an anesthetic, was found to inhibit L-type calcium channels (Ca.(L)) in human mesenteric artery cells. This effect was dose-dependent, suggesting a mechanism for its vasodilation properties.
Area of Science:
- Cardiovascular Pharmacology
- Smooth Muscle Physiology
- Anesthesiology
Background:
- Remifentanil is an ultra-short-acting opioid anesthetic known to induce vasodilation.
- The intracellular mechanisms of remifentanil-induced vasodilation may involve ion channel modulation.
- L-type calcium channels (Ca.(L)) play a critical role in vascular smooth muscle contraction.
Purpose of the Study:
- To investigate whether remifentanil inhibits Ca.(L) channels.
- To determine if remifentanil exerts dose-dependent effects on Ca.(L) currents (I(Ba.L)) in human mesenteric arterial smooth muscle cells.
Main Methods:
- Human mesenteric arterial smooth muscle cells were enzymatically isolated.
- Whole-cell patch-clamp technique was employed to analyze I(Ba.L).
- Cells were exposed to varying concentrations of remifentanil (1.21, 4.84, and 19.4 nmol.L(-1)) and compared to control.
Main Results:
- Remifentanil demonstrated a concentration-dependent blockade of I(Ba.L) with an IC(50) of 38.90 ± 3.96 x 10(-3) µmol.L(-1).
- The L-type calcium channel blocker, nifedipine, antagonized the remifentanil-induced currents.
- Remifentanil shifted the current-voltage relationship of I(Ba.L) in the hyperpolarizing direction.
Conclusions:
- Remifentanil significantly inhibits Ca.(L) channels in human mesenteric arteriolar smooth muscle cells.
- The inhibition of Ca.(L) channels by remifentanil is concentration-dependent.
- This finding provides insight into the cellular mechanisms underlying remifentanil's vasodilator effects.
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