Mepivacaine-induced contraction involves increased calcium sensitization mediated via Rho kinase and protein kinase C in endothelium-denuded rat aorta

Vascular endothelial over-expression of soluble epoxide hydrolase (Tie2-sEH) enhances adenosine A1 receptor-dependent contraction in mouse mesenteric arteries: role of ATP-sensitive K+ channels

“…Our data further revealed enhanced contraction to (Figure 1) in Tie2-sEH Tr mice. This increased trend of t-ERK expression (Figure 5C) in Tie2-sEH Tr mice may have possible link, such as in other studies, phosphorylation activates ERK1/2, which subsequently inhibits myosin light chain phosphatase, contributing to calcium sensitization and enhanced contraction [32, 33]. Thus, endothelial over-expression of sEH in MAs demonstrated enhanced vascular contractile responses to PE in Tie2-sEH Tr compared to WT mice.…”

Bupivacaine-induced Vasodilation Is Mediated by Decreased Calcium Sensitization in Isolated Endothelium-denuded Rat Aortas Precontracted with Phenylephrine

“…These results suggest that bupivacaine-induced relaxation may be associated with the inhibition of calcium sensitization involved in phenylephrine-induced contraction. In addition, Rho-kinase and protein kinase C inhibitors attenuate mepivacaine-induced vasoconstriction via the inhibition of calcium sensitization, suggesting that decreased calcium sensitization seems to be associated with vasodilation [15]. Because phenylephrine-induced contraction involves calcium sensitization associated with a pathway mediated by protein kinase C and Rho kinase, further research is needed regarding whether bupivacaine-induced vasodilation in aortas precontracted with phenylephrine may be associated with the inhibitory effect of bupivacaine on Rhokinase-and protein kinase C-mediated calcium sensitization induced by Rho-kinase activator NaF or protein kinase C activator phorbol 12,13-dibutyrate [21].…”

“…In addition, etomidate and alfentanil attenuate phenylephrine-induced contraction via an inhibitory effect on voltage-operated calcium channels [12,13]. Rho-kinase and protein kinase C are involved in the increased calcium sensitization, which lead to local anesthetic-induced vasoconstriction, whereas decreased calcium sensitization attenuates local anesthetic-induced vasoconstriction, which may be involved in vasodilation [6,14,15]. However, the cellular mechanism responsible for bupivacaine-induced relaxation in precontracted isolated rat aortas remains unknown.…”

Dexmedetomidine-Induced Contraction Involves CPI-17 Phosphorylation in Isolated Rat Aortas

“…Fura-2 loading and simultaneous measurements of [Ca 2+ ] i and tension were performed as described earlier [36]. Male Sprague-Dawley rats weighing 250–300 g were sacrificed by intraperitoneal administration of pentobarbital sodium (50 mg/mL) followed by exsanguination.…”