Cox R H, Folander K, Swanson R
Department of Physiology, University of Pennsylvania, Philadelphia, USA.
Hypertension. 2001 May;37(5):1315-22. doi: 10.1161/01.hyp.37.5.1315.
Voltage-gated K(+) currents play an important role in determining membrane potential, intracellular Ca(2+), and contraction in arterial smooth muscle. In this study, the expression of genes encoding voltage-gated K(+) channels of the Kv1.X family was compared in arteries from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Expression of Kv1.X in thoracic aorta, mesenteric arteries, tail artery, and heart was determined, both qualitatively and quantitatively, by reverse transcription-polymerase chain reaction. Our results demonstrate distinct but overlapping patterns of expression in vascular tissues. In general, Kv1.2 and Kv1.5 were most highly represented, and the levels of Kv1.2 were significantly larger in all tissues from SHR. Levels of Kv1.5 in arteries did not differ significantly between strains but were greater in SHR heart. Moderate levels of Kv1.3 and Kvbeta1.1 expression were also found in all tissues and were larger in SHR. Kv1.1 expression was not different between the 2 strains, and no significant expression of Kv1.4 (except in heart and aorta), Kv1.6, or Kvbeta2.1 was observed in either strain. Kv1.2 and Kv1.5 transcripts represent approximately 1 to 2 parts/10(5) of total mesenteric arterial RNA with approximately 2- to 5-fold lower levels in aorta and tail artery. Whole-cell voltage-gated K(+) channel currents, recorded from mesenteric arterial myocytes, were larger in SHR than WKY (eg, at 0 mV: 7.3+/-0.8 versus 10.9+/-1.2 pA/pF). The voltage dependence of activation was more negative in SHR (V(0.5): -20+/-4 mV versus -32+/-3 mV) but that of availability was not different. These results indicate that Kv1.X genes are differentially expressed between WKY and SHR (especially Kv1.2 and Kvbeta1.1). These differences in gene expression are associated with a greater voltage-gated K(+) channel current density in SHR and shifted voltage-dependent activation compared with WKY. These differences may be a compensatory mechanism related to the membrane potential depolarization in SHR or some manifestation thereof.
电压门控钾离子电流在决定动脉平滑肌的膜电位、细胞内钙离子浓度和收缩方面起着重要作用。在本研究中，比较了自发性高血压大鼠（SHR）和Wistar-Kyoto大鼠（WKY）动脉中编码Kv1.X家族电压门控钾离子通道的基因表达。通过逆转录-聚合酶链反应，定性和定量地测定了胸主动脉、肠系膜动脉、尾动脉和心脏中Kv1.X的表达。我们的结果表明，在血管组织中存在不同但重叠的表达模式。一般来说，Kv1.2和Kv1.5的表达最为显著，并且SHR所有组织中Kv1.2的水平显著更高。动脉中Kv1.5的水平在两个品系之间没有显著差异，但在SHR心脏中更高。在所有组织中也发现了中等水平的Kv1.3和Kvβ1.1表达，并且在SHR中更高。Kv1.1的表达在两个品系之间没有差异，并且在任一品系中均未观察到Kv1.4（心脏和主动脉除外）、Kv1.6或Kvβ2.1的显著表达。Kv1.2和Kv1.5转录本约占肠系膜动脉总RNA的1至2份/10⁵，在主动脉和尾动脉中的水平约低2至5倍。从肠系膜动脉肌细胞记录的全细胞膜电压门控钾离子通道电流，SHR比WKY更大（例如，在0 mV时：7.3±0.8对10.9±1.2 pA/pF）。SHR中激活的电压依赖性更负（V₀.₅：-20±4 mV对-32±3 mV），但可用性的电压依赖性没有差异。这些结果表明，WKY和SHR之间Kv1.X基因存在差异表达（尤其是Kv1.2和Kvβ1.1）。与WKY相比，这些基因表达差异与SHR中更大的电压门控钾离子通道电流密度和电压依赖性激活的改变有关。这些差异可能是与SHR膜电位去极化或其某些表现相关的一种补偿机制。
