ライフサイエンスコーパス: nisoldipine

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1 , which was partially inhibited by 10 microm nisoldipine.

2 The activity was not affected by nisoldipine.

3 voltage-gated Ca(2+) channel (VGCC) blocker nisoldipine (10 microM).

4 Nisoldipine (a DHP antagonist) blocks the smooth muscle

5 tion-contraction coupling in the presence of nisoldipine, a dihydropyridine Ca(2+) channel blocker, p

6 Nisoldipine, an inhibitor of VDCCs, reversed the effects

7 n is prevented by the Ca(2+) channel blocker nisoldipine and the K(+) channel opener pinacidil.

8 re with normal Ca2+ transport (nitrendipine, nisoldipine, Bay K 8644, A 23187) do not significantly a

9 ilitation" L-type Ca channels as revealed by nisoldipine blockade.

10 concentrations, and smoking behavior in the nisoldipine group (237 patients) and the enalapril group

11 mercaptopropionyl glycine; group II, n = 9), nisoldipine (group III, n = 6), or vehicle (group I [con

12 zed to intensive treatment with enalapril or nisoldipine had a mean 4-year blood pressure of 128+/-0.

13 We thus conclude that the more potent nisoldipine inhibition of smooth muscle versus cardiac L

14 nt and isoform-specific sensitivity of 10 nM nisoldipine inhibition of the channel were demonstrated,

15 inistration of a calcium-channel antagonist (nisoldipine) is as effective as antioxidant therapy in a

16 ment with either the calcium-channel blocker nisoldipine or the angiotensin-converting-enzyme inhibit

17 ltage-dependent Ca2+ channels (diltiazem and nisoldipine) or to the same extent by removal of externa

18 or L-type Ca2+ channel blockers (verapamil, nisoldipine, or cadmium) or by removal of extracellular

19 to therapy with the calcium-channel blocker nisoldipine than among those assigned to receive enalapr

20 In the nisoldipine-treated group, the total deficit of WTh on d

21 ment for cardiac risk factors, we found that nisoldipine was associated with a higher incidence of fa

22 The study also compared nisoldipine with enalapril as a first-line antihypertens

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