期刊
NEUROLOGICAL RESEARCH
卷 35, 期 4, 页码 424-428出版社
TAYLOR & FRANCIS LTD
DOI: 10.1179/1743132812Y.0000000129
关键词
L-type Ca2+ current; Nitric oxide; Patch clamp; Rabbit basilar artery; Sodium nitroprusside
资金
- Basic Science Research Program through the National Research Foundation of Korea (NRF)
- Ministry of Education, Science and Technology [2012R1A1A2003535]
- National Research Foundation of Korea [2012R1A1A2003535] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Objectives: Nitric oxide (NO) is well known to be a vasodilator, and NO donor compounds are currently used for treating vasospasm following subarachnoid hemorrhage. However, the action mechanism of cerebral vascular relaxation is not yet clear. L-type calcium channels have been determined to play an essential role in smooth muscle contraction. To investigate the role of L-type calcium channels in NO-induced relaxation of basilar smooth muscle cells, we examined the effect of the NO donor, sodium nitroprusside (SNP) on calcium (Ca2+) currents using smooth muscle cells isolated from a rabbit basilar artery. Method: The smooth muscle cells were isolated from rabbit basilar artery by enzyme treatment. To identify L-type Ca2+ currents, we used cesium chloride, a potassium channel blocker and Bay K8644, an activator of L-type Ca2+ channel. Results: The L-type calcium currents (91 +/- 13.0 pA; n=11) were significantly reduced by SNP (32 +/- 5 pA; n=11; P<0.05). 1H-[1,2,4] Oxadiazolo [4,3-a] quinoxalin-1-one, a 3',5'-cyclic guanosine monophosphate inhibitor, blocked the effect of SNP on L-type Ca2+ currents, and similar results were obtained after the application of 7-nitroindazole, a specific NO synthase inhibitor. Furthermore, inward currents were enhanced by Bay K8644 (170 +/- 22 pA; n=5) and were suppressed by SNP (54 +/- 13 pA; n=5; P<0.05). Discussion: These results demonstrate that NO suppresses the L-type Ca2+ currents in rabbit basilar smooth muscle cells, and suggest that L-type Ca2+ channels may play a pivotal role in NO-induced vascular relaxation.
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