Asano M, Masuzawa-Ito K, Matsuda T, Imaizumi Y, Watanabe M, Ito K
Department of Pharmacology, Nagoya City University Medical School, Japan.
Am J Physiol. 1993 Sep;265(3 Pt 2):H843-51. doi: 10.1152/ajpheart.1993.265.3.H843.
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 Ca(2+)-activated K+ (KCa) channels in the resting state of these arteries, the effects of agents that interact with these channels on tension and 86Rb 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 KCa channels, to the resting strips produced a concentration-dependent contraction in SHR but not in WKY. In resting strips preloaded with 86Rb, the basal 86Rb efflux rate constant was significantly greater in SHR than in WKY. The addition of nifedipine to the resting strips decreased the basal 86Rb efflux rate constant only in SHR. The effect of nifedipine on tension and 86Rb 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 45Ca 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 KCa channels were highly activated.
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主动张力；也就是说，加入硝苯地平后张力降低。为了确定Ca(2+)激活的K+（KCa）通道在这些动脉静息状态下的可能作用，比较了与这些通道相互作用的药物对SHR和正常血压的Wistar-Kyoto大鼠（WKY）颈动脉去内皮条带张力和86Rb外流的影响。向静息条带中加入高电导KCa通道阻滞剂蝎毒素，在SHR中产生浓度依赖性收缩，而在WKY中则不产生。在预先加载86Rb的静息条带中，SHR的基础86Rb外流速率常数显著高于WKY。向静息条带中加入硝苯地平仅在SHR中降低了基础86Rb外流速率常数。硝苯地平对WKY的25.9 mM K(+)收缩条带的张力和86Rb外流的影响与该阻滞剂对SHR静息条带的影响相当。与WKY相比，SHR静息条带中的基础45Ca内流显著增加，而硝苯地平消除了SHR中的这种增加。这些结果表明，在SHR颈动脉的静息状态下，通过L型电压依赖性Ca2+通道的跨膜Ca2+内流显著增加，并且KCa通道被高度激活。
