Abstract:

Objective〓〖WTBZ〗To explore the role of calcium in ropivacaine-induced contraction of vascular smooth muscle. 〖WTHZ〗Methods〓〖WTBZ〗Endothelium-denuded rat aortic rings and segments were prepared. The cumulative dose-contractile response relationships of aortic rings to ropivacaine were tested in the presence or absence of different concentrations of the L-type voltage-dependent calcium channel blocker, nicardipine, the inositol trisphosphate receptor blocker, 2-APB, or the lower extracellular calcium concentrations by using isometric force transducers. The cumulative dose-related increases in intracellular calcium concentration (［Ca2+］i) of aortic segments to ropivacaine were determined in the presence or absence of nicardipine, 2-APB, or the extracellular calcium-free by using a fluorimeter. 〖WTHZ〗Results〓〖WTBZ〗Ropivacaine induced a dose-dependent contractile response of rat aortic rings: increasing at concentrations of 0.03mmol/L to 0.3mmol/L and decreasing from 1 mmol/L to 3mmol/L, which was attenuated in a dose-dependent manner by nicardipine (1nmol/L, 5nmol/L and 10nmol/L), 2-APB (5μmol/L, 10μmol/L and 50μmol/L) and lower extra-cellular calcium concentrations (2mmol/L, 10mmol/L and 0). Ropivacaine also induced an increase in ［Ca2+］i in accordance with the contractile responses, which was also significantly inhibited by nicardipine (10?nmol/L), 2-APB (50μmol/L), and extra-cellular calcium-free. 〖WTHZ〗Conclusion〓〖WTBZ〗The increase in ［Ca2+］i by the extra-cellular calcium influx and the calcium release from the sarcoplasmic reticulum is involved in ropivacaine-induced vasoconstriction of rat aortic smooth muscle.

Key words: Ropivacaine, Vasoconstriction, Mechanism, calcium, Rat, Wistar