Muscarinic cholinergic regulation of L-type calcium channel in heart of embryonic mice at different

来源 :Acta Pharmacologica Sinica | 被引量 : 0次 | 上传用户:lywy0201
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AIM: To investigate the muscarinic regulation of L-type calcium current (ICa_L) during development. METHODS: The whole cell patch-clamp technique was used to record ICa_L in mice embryonic cardiomyocytes at different stages (the early developmental stage, EDS; the intermediate developmental stage, IDS; and the late developmental stage, LDS). Carbachol (CCh) was used to stimulate M-receptor in the embryonic cardiomyocytes of mice. RESULTS: The expression of 7Ca-L density did not change in different developmental stages (P>0.05). There was no difference in the sensitivity of ICa_L to CCh during development (P>0.05). This inhibitory action of CCh was mediated by inhibition of cyclic AMP since 8-bromo-cAMP completely reversed the muscarinic inhibitory action. IBMX, a non-selective inhibitor of phosphodiesterase (PDE), reversed the inhibitory action of M-receptor on 7Ca-L current by 71.2 %±9.2 % (n=8) and 11.3 %±2.5 % (n=9) in EDS and LDS respectively. However forskolin, an agonist of adenylyl cyclase (AC), METHODS: The whole cell patch-clamp technique was used to record ICa_L in mice embryonic cardiomyocytes at different stages (the early developmental stage, EDS; the intermediate Developmental stage, IDS; and the late developmental stage, LDS). Carbachol (CCh) was used to stimulate M-receptor in the embryonic cardiomyocytes of mice. RESULTS: The expression of 7Ca-L density did not change in different developmental stages > 0.05). There was no difference in the sensitivity of ICa_L to CCh during development (P> 0.05). This inhibitory action of CCh was mediated by inhibition of cyclic AMP since 8-bromo-cAMP-instituted AMPA inhibitor. IBMX, a non-selective inhibitor of phosphodiesterase (PDE), reversed the inhibitory action of M-receptor on 7Ca-L current by 71.2% ± 9.2% (n = 8) and 11.3% ± 2.5% (n = 9) in EDS and LDS respectively. However forskolin, an agonist of ade nylyl cyclase (AC),
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