FUNCTIONAL-ROLE OF CA-2+-ACTIVATED K plus CHANNELS IN RESTING STATE OF CAROTID ARTERIES FROM SHR

FUNCTIONAL-ROLE OF CA-2+-ACTIVATED K plus CHANNELS IN RESTING STATE OF CAROTID ARTERIES FROM SHR
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DOI:
10.1152/ajpheart.1993.265.3.h843
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发表时间:
1993-09-01
影响因子:
--
通讯作者:
ITO, K
ITO, K
中科院分区:
其他
文献类型:
--
作者:
ASANO, M;MASUZAWAITO, K;ITO, K

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自发性高血压大鼠(SHR)的颈动脉在暴露于生理盐溶液时表现出活跃的张力;即当加入硝苯地平时,张力降低。为了确定钙激活的钾(K(Ca))通道在这些动脉的静息状态中的可能作用,比较了与这些通道相互作用的药物对自发性高血压大鼠(SHR)和正常血压的Wistar-京都大鼠(WKY)去内皮颈动脉条张力和Rb-86外流的影响。在静息条上加入高电导K(Ca)通道阻断剂查氏毒素,可引起SHR的浓度依赖性收缩,但对WKY无此作用。在预加Rb-86的静息条上,SHR的基础Rb-86外流速率常数显著大于WKY。静息条中加入硝苯地平仅降低SHR基础Rb-86外流速率常数。硝苯地平对25.9 mm K+收缩的WKY条的张力和Rb-86外流的影响与该阻滞剂在SHR静息条上的作用相当。与WKY相比,SHR静息条基础Ca-45内流显著增加,这种增加可被硝苯地平所阻断。这些结果表明,在SHR颈动脉静息状态下,通过L型电压依赖性钙通道的跨膜钙内流显著增加,K(Ca)通道高度激活。
Carotid arteries from spontaneously hypertensive rats (SHR) exhibited an active tone when exposed to a physiological salt solution; that is, the tension decreased when nifedipine was added. To determine the possible role of Ca2+-activated K+ (K(Ca)) channels in the resting state of these arteries, the effects of agents that interact with these channels on tension and Rb-86 efflux were compared in endothelium-denuded strips of carotid arteries from SHR and normotensive Wistar-Kyoto rats (WKY). The addition of charybdotoxin, a blocker of high-conductance K(Ca) channels, to the resting strips produced a concentration-dependent contraction in SHR but not in WKY. In resting strips preloaded with Rb-86, the basal Rb-86 efflux rate constant was significantly greater in SHR than in WKY. The addition of nifedipine to the resting strips decreased the basal Rb-86 efflux rate constant only in SHR. The effect of nifedipine on tension and Rb-86 efflux in 25.9 mM K+-contracted strips of WKY was comparable to the effect of this blocker in the resting strips of SHR. The basal Ca-45 influx in resting strips of SHR was significantly increased when compared with WKY, and this increase in SHR was abolished by nifedipine. These results suggest that the transmembrane Ca2+ influx via L-type voltage-dependent Ca2+ channels was significantly increased in the resting state of carotid arteries from SHR and that the K(Ca) channels were highly activated.