ライフサイエンスコーパス: zaprinast

1 a does not attenuate the metabolic effect of Zaprinast.

2 .58A mutant has additional interactions with zaprinast.

3 il or UK-122764 is similar to that found for zaprinast.

4 h respect to Km for cGMP, kcat, and IC50 for zaprinast.

5 a cGMP-specific phosphodiesterase inhibitor, zaprinast.

6 s from CBDL rats, and intrarenal infusion of Zaprinast (10 micrograms/min) corrected the blunted incr

7 Inhibition of cGMP-specific PDE activity by zaprinast (10 microM, an inhibitor of PDE5 and PDE6) ind

8 ic GMP-specific phosphodiesterase inhibitor, zaprinast (20 mg/kg), resulted in significantly increase

9 with the type V phosphodiesterase inhibitor zaprinast (20 microm) plus the PKA inhibitor N-[2-(p-bro

10 tion for the PDE5 inhibitors, sildenafil, or zaprinast 3-isobutyl-1-methylxanthine.

11 allenge was performed and rats then received zaprinast (3 mg/kg bolus followed by 0.3 mg/kg/min infus

12 R6.58A increased the potency of zaprinast 30-fold in the pERK assay.

13 he orphan receptor GPR35 are kynurenic acid, zaprinast, 5-nitro-2-(3-phenylproplyamino) benzoic acid,

14 thine but is inhibited (IC50 = 35 microM) by zaprinast, a PDE5 inhibitor.

15 This dichotomy was recapitulated by zaprinast, a phosphodiesterase inhibitor that elevated c

16 Zaprinast, a specific competitive inhibitor of PDE, effe

17 In group 2, zaprinast administration did not alter hemodynamics.

18 logous to group 1 were then performed during zaprinast administration.

19 Zaprinast alone decreased the pulmonary hypertensive res

20 f CFRs was unaffected by NO, dipyridamole or zaprinast alone.

21 Zaprinast also significantly prolonged the permeability

22 We found Zaprinast alters the metabolomic profile of mitochondria

23 onses to both bradykinin and dimaprit, while zaprinast, an inhibitor of type 5 phosphodiesterase, pot

24 s inhibited by the selective PDE5 inhibitors zaprinast and DMPPO.

25 The combination of zaprinast and inhaled NO (either before or during hypoxi

26 3-4-5-6 for activation by the GPR35 agonists zaprinast and pamoic acid.

27 ine, 8-methoxymethyl isobutylmethylxanthine, zaprinast, and vinpocetine.

28 Both sildenafil and zaprinast are competitive inhibitors of PDE5, and double

29 First, a phosphodiesterase (PDE) inhibitor, Zaprinast, blocks inhibition by ATP.

30 Inhaled NO and zaprinast both decrease the pulmonary hypertensive respo

31 he cGMP-specific phosphodiesterase inhibitor zaprinast but not the inactive ST analog TJU 1-103.

32 ll dogs after they breathed NO combined with zaprinast (by 12.0+/-4.7 min [mean +/- SEM]) or dipyrida

33 blocking PDE by 3-isobutyl-1-methylxanthine/zaprinast caused significant inhibition of proliferation

34 he small artery segment after inhaled NO and zaprinast compared with NO alone.

35 The combination of inhaled NO and zaprinast decreased the total pressure decrease across t

36 ition, the phosphodiesterase (PDE) inhibitor zaprinast depolarized and occluded the NO-mediated depol

37 This metabolic effect of Zaprinast does not depend on inhibition of phosphodieste

38 sterase inhibitors isomethylbutylxanthine or Zaprinast (each at 10(-3) M) restored ANP responsiveness

39 , we found that the metabolic profile of the Zaprinast effect is nearly identical to that of inhibito

40 The cGMP phosphodiesterase inhibitor zaprinast enhanced the vasodilation response to lactate.

41 ophosphate phosphodiesterase inhibition with zaprinast enhances the effect of inhaled NO, particularl

42 constitute novel PKG inhibitors and prevent zaprinast from increasing cytosolic Ca(2+) The enhancers

43 or YC-1, and the phosphodiesterase inhibitor zaprinast greatly reduced spike frequency.

44 o 8-methoxymethyl isobutylmethylxanthine and zaprinast (IC(50) = 7.5 and 4.5 microM, respectively) an

45 on, and the cGMP phosphodiesterase inhibitor zaprinast, in wild-type and rd/rd mouse littermates to i

46 fil (but not 3-isobutyl-1-methylxanthine and zaprinast) induced a distinct conformational change in t

47 ,4)oxadiazolo[4,3-alpha]quinoxalin-1-one nor zaprinast influenced the cytostatic effect of NO or DFMO

48 Moreover, Zaprinast inhibits pyruvate-driven O2 consumption in bra

49 Infusion of Zaprinast into one renal artery in nephritic rats normal

50 h inhaled NO (20 ppm by volume), intravenous zaprinast, intravenous dipyridamole or the combination o

51 Zaprinast is a potent competitive inhibitor of cGB-PDE,

52 Our results show that Zaprinast is a potent inhibitor of mitochondrial pyruvat

53 Our findings show that Zaprinast is a specific mitochondrial pyruvate carrier (

54 Zaprinast is a well known phosphodiesterase inhibitor an

55 enafil (Ki = 1 nM) > UK-122764 (Ki = 5 nM) > zaprinast (Ki = 130 nM)].

56 udied with inhaled NO only, with infusion of zaprinast only (0.25 mg/kg bolus and 0.05 mg/kg/min infu

57 specific activity, Km for cGMP, and IC50 for zaprinast or 3-isobutyl-1-methylxanthine were found amon

58 intracellular Ca(2+) stores independently of zaprinast or PKG.

59 es C) or STH containing rolipram, milrinone, zaprinast, or theophylline.

60 g features of the standard surrogate agonist zaprinast, or with lodoxamide and bufrolin, were also sh

61 he specific cGMP phosphodiesterase inhibitor zaprinast reduced the frequency of spontaneous pacemaker

62 es of 0.82 and 5 microM for dipyridamole and zaprinast, respectively.

63 esence of 10(-3) M isobutylmethylxanthine or Zaprinast, two different inhibitors of cyclic nucleotide

64 sitivity of H257N to a competitive inhibitor zaprinast was also unaffected.

65 Zaprinast was the only drug that inhibited PDE6 more pot

66 and erectile responses to acetylcholine and zaprinast were enhanced at a time when the erectile resp

67 V cGMP-selective phosphodiesterase inhibitor zaprinast were enhanced, whereas systemic responses were

68 advantage of the phosphodiesterase inhibitor zaprinast, which we show acts in part through cGMP-depen

69 damole, with an IC(50) of 1.8 microM, and to zaprinast, with an IC(50) of 28 microM.

70 elective inhibitor of cGMP-phosphodiesterase zaprinast (ZAP), caused an inhibition of RA.