ライフサイエンスコーパス: cromakalim

1 he potent vasodilating K(ATP) openers (e.g., cromakalim).

2 tereoselective for the (3S,4R)-enantiomer of cromakalim.

3 -sensitive potassium (K(ATP)) channel opener cromakalim.

4 4-fold by pinacidil (1 mM) and unaffected by cromakalim (0.5 mM).

5 ic bladder overactivity, compound 14 and (-)-cromakalim 1 were found to inhibit spontaneous bladder c

6 As for cromakalim (1) and 2, the cardioprotective effects of co

7 ctive for the ischemic myocardium than 2 and cromakalim (1), respectively.

8 ers of magnitude more cardiac selective than cromakalim (1).

9 ed to 2 and the first-generation KATP opener cromakalim (1).

10 (13+/-1 and 23+/-1 vs. 4+/-1 and 10+/-2% for cromakalim 10(-8), 10(-6) M before and after vasopressin

11 FPI-indomethacin pretreated for responses to cromakalim 10(-8), 10(-6) M, respectively).

12 +/-2%, FPI-MEAVP pretreated for responses to cromakalim 10(-8), 10(-6) M, respectively).

13 Cromakalim (10 micromol/L), an ATP-sensitive potassium c

14 microM) as well as by the K+ channel openers cromakalim (20 microM) and diazoxide (10 microM).

15 ither ML-7 (0.5 mm) to block contraction, or cromakalim (3 mum) to hyperpolarize the downstream muscl

16 l microsuffusion of the KATP channel agonist cromakalim (5 nmol), whereas it had no effect on the 103

17 nylurea receptor SUR1 subunits, but not with cromakalim, a selective opener for SUR2-based channels,

18 lation by H2O2, glutamate, and GABA, whereas cromakalim, a SUR2-selective opener, did not.

19 adenylate cyclase activating polypeptide and cromakalim, adenylate cyclase and K(ATP) channel activat

20 lim (K1/2 = 1 microM), and two developmental cromakalim analogues, EMD60480 and EMD57970 (K1/2 = 6 nM

21 The potassium channel openers cromakalim and BMS-180448 were competitive inhibitors of

22 We also determined the effects of cromakalim and diazoxide on reconstituted rat mitochondr

23 Cromakalim and diazoxide were both potent activators of

24 ptide derivatives of the KATP channel opener cromakalim and evaluated their IOP lowering capabilities

25 with the K(ATP) and K(ca) channel agonists, cromakalim and NS1619 (10(-8), 10(-6) M) diminished dila

26 d with the K(ATP) and K(ca) channel agonists cromakalim and NS1619 in a concentration approximating t

27 Cromakalim and NS1619 induced pial artery dilation was a

28 Cromakalim and NS1619 induced pial artery dilation was a

29 huSUR2A/huKIR6.2 channels were stimulated by cromakalim and pinacidil in the presence of ATP and Mg2+

30 ponses, elicited by acetylcholine, iloprost, cromakalim, and elevated [K+], were greatly diminished i

31 K(ATP) channel openers (minoxidil, cromakalim, and pinacidil) increased cellular DNA synthe

32 2-17, confers sensitivity to the benzopyran, cromakalim, and the pyridine, pinacidil, whereas an SUR1

33 n potential duration significantly less than cromakalim at equicardioprotective concentrations.

34 ed vasodilation induced by the Katp agonists cromakalim, calcitonin gene related peptide (CGRP) and t

35 ening APD to a comparable degree as hypoxia, cromakalim failed to induce net tissue K loss, ruling ou

36 -1,1-diamin e (Bay X 9228) > pinacidil > (-)-cromakalim > N-(4-benzoyl phenyl)-3,3,3-trifluro-2-hydro

37 r to KATP channel openers like diazoxide and cromakalim in heart, liver, and brain mitochondria.

38 diazoxide was significantly less potent than cromakalim in increasing sarcolemmal K+ currents.

39 . 4+/-1 and 10+/-2 vs. 8+/-1 and 19+/-1% for cromakalim in untreated, vasopressin, and vasopressin pl

40 Cromakalim increased (P<0.01) the vulnerability (product

41 Diazoxide and cromakalim increased the time to onset of contracture wi

42 nophore valinomycin or the K+-channel opener cromakalim induced apoptosis.

43 s restored by diazoxide (K1/2 = 0.4 microM), cromakalim (K1/2 = 1 microM), and two developmental crom

44 ning the effects of the KATP channel agonist cromakalim on unidirectional K efflux, total tissue K co

45 of sarcolemmal versus beta-cell channels to cromakalim or pinacidil versus diazoxide.

46 Furthermore, hyperpolarization induced with cromakalim or valinomycin significantly reduced both 5-H

47 ized by the ATP-sensitive K+ channel openers cromakalim, pinacidil, or diazoxide.

48 ide and U-37883A and the KATP channel opener cromakalim suggested that venular, unlike arteriolar, sm

49 mpare cardioprotective potency, diazoxide or cromakalim was given to isolated rat hearts subjected to

50 These effects of cromakalim were reversible.