ライフサイエンスコーパス: SA node

1 connecting LA GPs with the PVs, AV node, and SA node.

2 xtends beyond the AV node to also affect the SA node.

3 e, whereas Nav1.1 was present throughout the SA node.

4 )1.1 alpha subunits were also present in rat SA node.

5 gesting that the deficit is intrinsic to the SA node.

6 vity between the periphery and center of the SA node.

7 cells but was absent from the center of the SA node.

8 ocytes of the ventricles and the sinoatrial (SA) node.

9 ich is expressed in atrial tissue but not in SA node), and Na(+) channel localization was analyzed by

10 re are no atrial cells within the functional SA node, and the differences result from a change in the

11 king since the rate of beating of guinea-pig SA node/atrial preparations was slowed in the presence o

12 all four beta subunits were present in mouse SA node, but Na(v)1.5 alpha subunits were not.

13 ed: Nav1.5 was absent from the centre of the SA node, but present in the periphery of the SA node, wh

14 alpha(1D)) Ca(2+) channel in the sinoatrial (SA) node by using Ca(v)1.3 Ca(2+) channel-deficient mice

15 t on purinoceptors on cardiomyocytes, AV and SA nodes, cardiac fibroblasts, and coronary blood vessel

16 ice designated randomly as an atrial cell or SA node cell (in correct proportions for periphery and c

17 , two important pacemaker currents in rabbit SA node cells and point to both I(Ca.T) and I(Ca.L) as m

18 rents (I(Ca,L)s) recorded in single isolated SA node cells from Ca(v)1.3(-/-) mice show a significant

19 hange in the mix of atrial cells and uniform SA node cells from periphery to center, whereas accordin

20 from a change in the intrinsic properties of SA node cells from periphery to center.

21 oth intact SA node preparations and isolated SA node cells without a significant effect on SA node co

22 In freshly dissociated rabbit single SA node cells, inhibition of CaMKII by a specific peptid

23 P and 3 micromol/L KN-93 completely arrested SA node cells, which indicates that basal CaMKII activat

24 nd action potentials (APs) from young rabbit SA node cells.

25 ficantly contribute to spontaneous pacing in SA node cells.

26 ation of the spontaneous action potential in SA node cells.

27 ontaneous rhythmic excitation of sinoatrial (SA) node cells.

28 TX-sensitive iNa, slowed both pacemaking and SA node conduction.

29 A node cells without a significant effect on SA node conduction.

30 The SA node contained 25 times the total HCN message of Purk

31 ough L-type Ca2+ channels in the sinoatrial (SA) node contributes to pacemaker activity, whereas L-ty

32 tivity of pacemaker cells in the sinoatrial (SA) node controls heart rate under normal physiological

33 that Ca(v)1.2 protein expression within the SA node declined during aging.

34 ker activity, in turn leading to age-related SA node degeneration.

35 lined within the center and periphery of the SA node during aging.

36 Clinical studies have shown the incidence of SA node dysfunction increases with age and occurs with p

37 saic model) of the makeup of the sinoatrial (SA) node has been proposed to explain the characteristic

38 CBP60g/SARD1 node between the PAD4/EDS1 and SA nodes in the defense signaling network, and indicated

39 c model of the SA node is untenable, and the SA node is adequately described by the gradient model.

40 The mosaic model of the SA node is untenable, and the SA node is adequately desc

41 origin of the heartbeat in the sino-atrial (SA) node is usually thought to arise from the sequential

42 rms are important for the functioning of the SA node: neuronal (putative Nav1.1) and cardiac Nav1.5 i

43 Similar to the I(Ca,L) recorded in the SA node of Ca(v)1.3(-/-) mutant mice, the Ca(v)1.2 Ca(2+

44 Here we report that SA node pacemaker activity is critically dependent on Ca

45 In the present study, in mouse SA node pacemaker cells, we investigated Na+ currents un

46 e to membrane depolarization participates in SA node pacemaker currents, but their role in the workin

47 sitive iNa, slowed pacemaking in both intact SA node preparations and isolated SA node cells without

48 ty to the L-type calcium blocker nifedipine; SA node preparations stopped beating in 100 micromol/L n

49 The SA node region was isolated from the right atrium of gui

50 cally isolated myocytes from the sinoatrial (SA) node, right and left atria, right and left ventricle

51 ntaneous action potentials recorded from the SA nodes show a significant decrease in the beating freq

52 In the rabbit SA node, the dominant HCN transcript is HCN4, representi

53 propagation of the action potential from the SA node to the surrounding atrial muscle.

54 ting that neural pathways from the LA to the SA node travel via the right upper GP.

55 SA node, but present in the periphery of the SA node, whereas Nav1.1 was present throughout the SA no

56 tly with reduced spontaneous activity of the SA node with increased age, which provides further evide