Effects of isoflurane on receptor-operated Ca2+ channels in rat aortic smooth muscle

Abstract

We have investigated the effects of isoflurane on receptor-operated Ca2+ channels (ROC) in vascular smooth muscle. In isolated rat thoracic aortic rings denuded of endothelium, the effects of isoflurane on phenylephrine-induced contraction and Ca2+ influx were evaluated in the presence of supramaximal doses of nifedipine or verapamil. Under isometric tension recording, the aortic rings were precontracted by phenylephrine 300 nmol litre-1 and exposed to 1.2%, 2.3% or 3.5% isoflurane. Phenylephrine-induced precontraction was enhanced with 2.3% isoflurane by mean 8.1 (SD 9.3)% (P < 0.05 vs 0% isoflurane). The constrictor effect of 2.3% isoflurane was not inhibited by depletion of intracellular Ca2+ stores with ryanodine 20 mumol litre-1, but was abolished in a Ca(2+)-free solution or by SK&F 96,365 30 mumol litre-1, an ROC blocker. Isoflurane-induced contraction was accompanied by increased intracellular free Ca2+ concentration, monitored using fura PE3. Unidirectional 45Ca2+ influx measurement in phenylephrine-stimulated aortic strips revealed that the mean amount of Ca2+ influx was significantly (P < 0.05) enhanced by 1.2% and 2.3% isoflurane, which were 117.1% and 119.7% of control values, respectively. Our results strongly suggest that isoflurane enhanced Ca2+ influx through ROC that had been submaximally activated by phenylephrine.

Erythroxylum pungens elicits vasorelaxation by reducing intracellular calcium concentration in vascular smooth muscle cells of rats

“…Contractions of vascular smooth muscle cells induced by KCl (80 mM) rely almost exclusively on Ca 2+ infl ux through activation of voltage-sensitive channels, (Hirata et al, 1998), whereas contractions induced by Phe are mediated by an increase in Ca 2+ infl ux through both receptor-operated channels with findings reported by others Bastos et al, 2010;Cavalcante et al, 2011). However, this result does not rule out the possibility that EEEP interferes with the sarco-endoplasmatic reticulum Ca 2+ -ATPases.…”

Endothelium-independent vasodilation induced by kolaviron, a biflavonoid complex from Garcinia kola seeds, in rat superior mesenteric arteries

“…*, Significantly different from control (P<0.05), ANOVA followed by Dunnett's multiple comparison test. (Hirata et al, 1998), whereas contractions induced by PHE are mediated by an increase in Ca 2+ influx through both receptor-operated channels (Lee et al, 2001a) and voltage-sensitive channels (Eckert et al, 2000;Lee et al, 2001b (Leijten and van Breemen, 1984), whereas, the caffeine-induced contractions, which releases [Ca 2+ ]i by an (IP3)-independent mechanism (Standen et al, 1989) were unaltered. Thus, it seems likely that the vascular effects of KV involve a reduction in Ca 2+ release from In order to analyze the contribution of different types of K + channels to the KV-induced endothelium-independent relaxation in the mesenteric rings, we used agents that are known to possess a K + channel-blocking activity.…”

Aging and total stenosis triggers differential responses of carotid and basilar arteries to endothelin-1 and phenylephrine

“…Interestingly, the reduced reactivity to endothelin-1 is not due to a reduction of contractile machinery of the stenosed guinea pig carotid, since the contractile response of these arteries to phenylephrine, a selective α1-adrenoreceptor agonist, and KCl, a depolarizing agent, was also reduced by stenosis. Contractions of vascular tissues induced by KCl rely almost exclusively on Ca 2+ influx through activation of voltage-sensitive channels (Hudgins and Weiss, 1968), whereas contractions induced by phenylephrine are mediated by an increase in Ca 2+ influx through both receptor-operated channels (Hirata et al, 1998) and voltage-sensitive channels (Wesselman et al 1996;Lee et al, 2001). Likewise, endothelin-1-induced contraction involves the influx of extracellular Ca 2+ through receptor-operated and voltage-sensitive Ca 2+ channels (Rubany et al 1994).…”