Nitric oxide increases the activity of the apical 70-pS K+ channel in TAL of rat kidney

被引:42
作者
Lu, M [1 ]
Wang, XH [1 ]
Wang, WH [1 ]
机构
[1] New York Med Coll, Dept Pharmacol, Valhalla, NY 10595 USA
关键词
guanosine; 3; 5 '-cyclic monophosphate; nitric oxide synthase; patch clamp; rat kidney;
D O I
10.1152/ajprenal.1998.274.5.F946
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
We have previously shown that nitric oxide (NO) mediates the stimulatory effect of angiotensin II on the apical 70-pS K+ channel in the thick ascending limb (TAL) of Henle's loop of the rat kidney (12). In the present study, we used the patch-clamp technique to examine the effects of NO on the 70-pS K+ channel. Addition of 10 mu M S-nitroso-N-acetylpenicillamine (SNAP), a NO donor, increased the channel activity in cell-attached patches. In contrast, application of 100 mu M N-omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase (NOS), reduced the channel activity by 75 +/- 7%. The effect of L-NAME was the result of inhibiting NOS, since D-NAME, which does not block NOS activity, had no effect on the channel activity. In addition, the effect of L-NAME was abolished in the presence of 1 mM L-arginine or by addition of 10 mu M SNAP, further supporting the role of NO. Finally, the L-NAME-induced inhibition was also reversed by adding 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP). That the effect of NO is mediated by the cGMP-dependent pathway is also suggested by experiments in which inhibition of guanylate cyclase abolished the effect of SNAP. Finally, 10 mu M SNAP significantly increased cGMP concentration of the medullary TAL from 12.4 fM/mu g protein to 38.9 fM/mu g protein, as measured with ELISA. We conclude that NO is involved in regulating the activity of the apical 70-pS K+ channel in the TAL of the rat kidney.
引用
收藏
页码:F946 / F950
页数:5
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