ライフサイエンスコーパス: inotropy

1 ve nitrosylation, thiol reactivity, positive inotropy).

2 nase A (PKA) is critical for skeletal muscle inotropy.

3 gnaling and normalize beta1AR expression and inotropy.

4 serine phosphorylation of Akt, and negative inotropy.

5 ibution to caveolae, with diminished cardiac inotropy.

6 parasympathetic control of left ventricular inotropy.

7 rom heavier endosomes while retaining normal inotropy.

8 nomena of rest decay and frequency-dependent inotropy.

9 CE, SKF96365, was also effective in blunting inotropy.

10 ce of tonic inhibitory vagal influence on LV inotropy.

11 allows NO to inhibit beta-adrenergic-induced inotropy.

12 ptors (ARs) in the heart results in positive inotropy.

13 d mechanism of beta-AR modulation of cardiac inotropy.

14 c inhibitory muscarinic influence on cardiac inotropy.

15 ucagon receptors) play a key role in cardiac inotropy.

16 a cascade leading to cardiac chronotropy and inotropy.

17 doses did not induce myocyte death or affect inotropy.

18 t-bound receptors, have increased myocardial inotropy.

19 alternative mechanisms of glycoside-induced inotropy: (1) direct activation of sarcoplasmic reticulu

20 rtrophy and depressed stimulation of cardiac inotropy and chronotropy by beta-adrenergic receptor (be

21 rgic receptors (ARs) are GPCRs that regulate inotropy and chronotropy in the heart and mediate vasodi

22 in the mouse, beta-AR stimulation of cardiac inotropy and chronotropy is mediated almost exclusively

23 tally exerts the same directional effects on inotropy and chronotropy, albeit through different mecha

24 (beta2AR), an important modulator of cardiac inotropy and chronotropy, has significant genetic hetero

25 th the attenuated beta-adrenoceptor-mediated inotropy and chronotropy.

26 red responses to BAY y 5959, which increases inotropy and decreases chronotropy, with those to norepi

27 ng that under conditions of positive cardiac inotropy and enhanced efficiency of EC coupling alternan

28 nol stimulation but had minimal effect on AS inotropy and enhanced lusitropy.

29 s of this agent include a modest increase in inotropy and improvement in diastolic function, both of

30 S3(-/-)+AdVbeta(gal) mice displayed enhanced inotropy and lusitropy over WT at slower heart rates but

31 L-NIL dramatically increased the ISO-induced inotropy and lusitropy, such that the ISO+AG response in

32 d marked augmentation of frequency-dependent inotropy and relaxation, with a peak frequency response

33 nitric oxide (NO), induces positive cardiac inotropy and selective venodilation in the normal in viv

34 fects of T(3) can contribute to the positive inotropy and sinus (atrial) tachycardia traditionally at

35 of atrial 5-HT4 receptors produces positive inotropy and tachycardia that can precipitate arrhythmia

36 Both cardiac inotropy and the progression of heart disease are affect

37 We hypothesize that this inotropy and the resulting increase in tissue blood flow

38 nderlying this chronic IL-6-induced negative inotropy and the role of iNOS.

39 cluding a 2.6x increase in systolic calcium (inotropy) and a 28% decrease in calcium half-relaxation

40 factors were derived: 1) parasympathetic, 2) inotropy, and 3) systemic vascular resistance.

41 AD thus had negative effects on chronotropy, inotropy, and lusitropy, thereby indicating a key role f

42 ator of at least a component of the positive inotropy associated with agents that stimulate phospholi

43 These studies demonstrate a negative inotropy associated with jet ventilation that, during he

44 mechanism for chronic IL-6-induced negative inotropy at 2 h, both sGC/cGMP/PKG and ONOO-, at least i

45 nearly fully inhibited isoproterenol-induced inotropy) but not partial beta-blockade.

46 AS-induced positive inotropy, but not systemic vasodilatation, was highly re

47 ence of a new molecular pathway for positive inotropy by a cardiac-restricted microRNA (miR).

48 myofilament-based molecular manipulation of inotropy by histidine-modified troponin I maintains card

49 igher sensitivity to isoprenaline-stimulated inotropy compared with control subjects.

50 The time to peak inotropy for both phases depended on the light intensity

51 Glycoside-induced cardiac inotropy has traditionally been attributed to direct Na(

52 es lymphatic contractions stronger (enhanced inotropy - higher contraction amplitude) and propels mor

53 aptan], and adenosine) and non-cAMP-mediated inotropy (ie, levosimendan), are currently under investi

54 ite (ONOO-) in chronic IL-6-induced negative inotropy in ARVM.

55 ions of ouabain resulted in positive cardiac inotropy in both isolated hearts and intact animals expr

56 ng EMD-57033 dose further augmented positive inotropy in CON and HF, accompanied by vasodilation, inc

57 Acetylcholine reversed isoproterenol inotropy in controls (108+/-21% reduction of +dP/dt resp

58 thereby partially normalize beta-adrenergic inotropy in DM phospholamban mice.

59 a novel form of calcium-independent positive inotropy in failing cardiac myocytes by fast alpha-myosi

60 pe mice, cTnI(PKC-P) mice exhibited negative inotropy in isolated hearts (14% decrease in peak develo

61 the regulation of basal and beta-adrenergic inotropy in normal and chronically infarcted hearts.

62 sfer can confer calcium-independent positive inotropy in slow beta-myosin-dominant rabbit and human f

63 or physiological mechanisms of modulation of inotropy in the heart.

64 nhibition augmented isoproterenol-stimulated inotropy in wild-type (WT), but not in beta(3)(-/-) mice

65 (lusitropy), and increased force production (inotropy) in response to epinephrine.

66 ed, and to prevent excessive ssTnI-dependent inotropy (increased Ca(2+) sensitivity) in the embryonic

67 Peak aortic acceleration (LV inotropy) increased by 0.8 g in EA but only by 0.2 g in

68 The underlying mechanism of the positive inotropy incurred with L-755,507 in the TGbeta(3) mice w

69 These treatments did not inhibit inotropy induced by activation of adenylate cyclase thro

70 Thus, CGRP-mediated positive inotropy is load-independent but indirect and attributab

71 of nitric oxide (NO), exert positive cardiac inotropy/lusitropy in vivo and in vitro, due in part to

72 ique cardiovascular features (i.e., positive inotropy/lusitropy) that may have relevance for pharmaco

73 However, their negative chronotropy and inotropy may potentially lead to an inappropriately low

74 Myofilament-based inotropy may represent a therapeutic avenue to improve m

75 ls demonstrated that ouabain-induced cardiac inotropy occurred in hearts from wild type but not from

76 Enhancement of contractile force (inotropy) occurs in skeletal muscle following neuroendoc

77 sion of human beta(3)ARs results in positive inotropy only on stimulation with a beta(3)AR agonist.

78 Molecular inotropy refers to cardiac contractility that can be mod

79 lecular mechanism underlying skeletal muscle inotropy requires enhanced SR Ca(2+) release due to PKA

80 e (NO) production, which attenuates positive inotropy, suggesting a possible negative feedback mechan

81 on and were studied under varying degrees of inotropy (using increasing extracellular calcium [Ca2+]o

82 y alter cardiac muscle contraction: negative inotropy via decreased cross-bridge formation and negati

83 ne hydrochloride (L-NMMA) on beta-adrenergic inotropy was assessed in conscious dogs before and after

84 ion were similar, beta-adrenergic-stimulated inotropy was increased in beta(3)(-/-) mice, and similar

85 CGRP-positive inotropy was not attributable to reflex activation becau

86 on by hyperglycemia of phenylephrine-induced inotropy was reversed with azaserine and mimicked by glu

87 se isozyme, mediates ouabain-induced cardiac inotropy, we developed animals expressing a ouabain-inse