LAI Donna;ALLEN David;
<正>The sinoatrial node(SAN)is the primary pacemaker of the mammalian heart.Dysfunction of the SAN increases exponentially with age.The age-related remodelling of pacemaker currents and pacemaker action potential may contribute to age-related slowing of the heart rate and reduction in conduction velocity which result in arrhythmias.We recently discovered that store-operated Ca~(2+) channel(SOCC)activity is present in the mouse sinoatrial node leading to Ca~(2+) entry.In the present study we tested the hypotheses that changes in SOCC activity might play a significant role in aging related SAN dysfunction.The experiments were carried out in intact mouse SAN preparations from either adult(2 months)or old(>18 months)mice.Intracellular Ca~(2+) was detected with the fluorescent Ca~(2+) indicator indo-1.The SOCC activity was determined from the influx of Ca~(2+) following depletion of the sarcoplasmic reticulum Ca~(2+) store.We found that the Ca~(2+) influx was reduced in old mice compare to adult mice (2 month)(P<0.05,n=4).It is general believed that the transient receptor potential channel(TRPCs)gene family are candidates for encoding SOCC.Using CellDirect one-step qRT-PCR method,we detected a downregulation of the mRNA expression of TRPCs(TRPC1,3,and 4)in the SANs from old mice(20-24 months),compare to the ones from young mice(1 month).However,the differences so far are not significant.This may reflect limited sample size or increased variability of the reference gene expression in aging mouse heart.Our preliminary data suggest that changes in SOCC activity and expression of TRPC genes might play a role in SAN dysfunction, specifically in the aging heart.
store-operated Ca~(2+)channel;;TRPC;;sinoatrial node;;aging
To explore the background and basis of the node document
Documents that have the similar content to the node document