Relaxant effect of the aqueous extract of Erythrina vellutina leaves on rat vas deferens

The effect of the Aqueous Extract from the leaves of Erythrina vellutina (AE) on rat vas deferens preparation was evaluated in this work. The AE inhibited the muscle contractions induced by electrical field stimulation (EFS) in a concentration-dependent manner. This inhibition was not affected by atropine (10-5M), propanolol (10-5M), prazosin (10-5M) or yohimbine (10-5M), suggesting that there is no direct interaction of the AE with cholinergic nor adrenergic receptors. Incubation of vas deferens with the K+ channel antagonists, tetraethylamonium (10-6M) or 4-aminopyridine (10-6M) had also no effect on the AE-induced inhibition. On the other hand, glibenclamide (10-6) significantly attenuated the effect of the AE, suggesting a possible involvement of ATP-dependent K+ channels. The AE (0.15 mg/mL) did not alter the contractions induced by noradrenaline (10-5M), ATP (10-4M) nor KCl (80 mM), against an interaction of the extract with post-synaptic sites. The data presented suggests that the inhibition of the electrically driven muscle twitches by the AE could be due to a pre-synaptic interaction of the extract with ATP-dependent K+ channels from vas deferens sympathetic neurons.

O objetivo deste trabalho foi avaliar o efeito do extrato aquoso das folhas de Erythrina vellutina (AE) sobre ducto deferente de rato. Nesta preparação, o AE inibiu as contrações induzidas por estímulo elétrico de campo de maneira dependente da concentração. Esta inibição não foi afetada após atropina (10-5M), propanolol (10-5M), prazosin (10-5M) ou yohimbina (10-5M), sugerindo uma ação indireta do AE sobre receptores colinérgicos ou adrenérgicos. A incubação da preparação com os antagonistas de canais de K+, tetraetilâmonio (10-6M) ou 4-aminopiridina (10-6M) não alterou o efeito inibitório induzido pelo AE. Entretanto, a glibenclamida (10-6M) atenuou significantemente este efeito, sugerindo um possível envolvimento de canais de K+ dependentes de ATP. Além disso, o AE (0.15 mg/mL) não alterou as contrações induzidas por noradrenalina (10-5M), ATP (10-4M) ou KCl (80 mM), descartando uma interação do AE com um sítio pós-sináptico. Em conclusão, estes resultados demonstram que o efeito inibitório do AE pode ser devido a uma interação pré-sináptica com canais de K+ dependentes de ATP em neurônios simpáticos de ducto deferente de rato.

Effects of Propofol on Hypoxic Pulmonary Vasoconstriction after Pretreatment with L-NAME and Glibenclamide in Isolated Rat Lungs / 대한마취과학회지

BACKGROUND: It is generally accepted that propofol does not inhibit hypoxic pulmonary vasoconstriction (HPV). However, because the previous studies for the effects of propofol on HPV were established in vivo, the effects of physiologic variables could not be ruled out. Therefore, we investigated the effects of various concentrations of propofol on HPV at isolated rat lungs and the relationship of these effects of propofol on HPV and endothelium-derived relaxing factor (EDRF) and an ATP-dependent K+ channel which were candidates as the mechanism of HPV. METHODS: In 30 isolated rat lungs, after three hypoxic challenges for 5 minutes, we administered saline in the control group, N(G)-nitro-L-arginine methyl ester (L-NAME) in the L group and glibenclamide in the G group followed by three hypoxic challenges for 5 minutes. In addition, we studied the effects of various concentrations of propofol on HPV in the three groups. RESULTS: L-NAME and glibenclamide did not alter baseline pulmonary arterial pressure but L-NAME significantly enhanced HPV. Clinical concentrations of propofol did not affect HPV and high concentrations of propofol inhibited HPV. The pretreatment of L-NAME and glibenclamide did not alter the inhibition of HPV even at high concentrations of propofol. CONCLUSIONS: The EDRF and ATP-dependent K+ channel did not largely contribute to baseline pulmonary arterial tone but EDRF might be released and downregulate HPV. Clinical concentrations of propofol did not inhibit HPV but high concentrations of propofol inhibited HPV. In addition, the mechanism of inhibition of HPV at high concentrations of propofol did not relate to the EDRF pathway and ATP-dependent K+ channel.