Martens J R, Gelband C H
Department of Physiology, University of Florida College of Medicine, Gainesville 32610-0274, USA.
Circ Res. 1996 Aug;79(2):295-301. doi: 10.1161/01.res.79.2.295.
The renal vasculature plays an important role in the control of blood pressure. K+ channels have been demonstrated to regulate smooth muscle membrane potential and thereby control smooth muscle tone. However, few data are available on K+ channel function in the renal vasculature of hypertensive animals. This study details changes in K+ currents and membrane potential in genetic and nongenetic models of hypertension. The patch-clamp technique and Ca(2+)-imaging fluorescence were used to examine the differences in Wistar-Kyoto (WKY), Sprague-Dawley (SD), spontaneously hypertensive (SHR), and deoxycorticosterone acetate (DOCA) hypertensive single cells of rat kidney interlobar arteries. In current-clamp experiments, SHR and DOCA hypertensive cells were approximately 20 mV more depolarized than the control cells. In voltage-clamp experiments with 4-amino-pyridine and niflumic acid present to inhibit voltage-dependent K+ (K(v)) and Ca(2+)-activated CI- (CI(Ca)) currents, SHR and DOCA hypertensive Ca(2+)-activated K+ (K(Ca)) currents were significantly larger and activated at more negative potentials than the control. Conversely, with charybdotoxin and niflumic acid present to inhibit K(Ca) and CI(Ca) currents, SHR and DOCA hypertensive K(v) current was significantly smaller than the control. Finally, basal and angiotensin II-stimulated peak intracellular free [Ca2+] was greater in the SHR and DOCA hypertensive cells compared with control cells. These results suggest that membrane potential and the activity of K(Ca) and K(v) channels are altered in hypertensive rat renal interlobar arteries and may play a role in the regulation of renal blood flow under physiological and patho-physiological conditions.
肾血管系统在血压控制中发挥着重要作用。钾通道已被证明可调节平滑肌膜电位，从而控制平滑肌张力。然而，关于高血压动物肾血管系统中钾通道功能的数据却很少。本研究详细阐述了高血压遗传和非遗传模型中钾电流和膜电位的变化。采用膜片钳技术和钙成像荧光法检测大鼠肾叶间动脉的Wistar-Kyoto（WKY）、Sprague-Dawley（SD）、自发性高血压（SHR）和醋酸脱氧皮质酮（DOCA）高血压单细胞的差异。在电流钳实验中，SHR和DOCA高血压细胞的去极化程度比对照细胞大约高20 mV。在电压钳实验中，加入4-氨基吡啶和氟灭酸以抑制电压依赖性钾（K(v)）和钙激活氯（Cl(Ca)）电流，SHR和DOCA高血压细胞的钙激活钾（K(Ca)）电流明显更大，且在比对照更负的电位下激活。相反，加入蝎毒素和氟灭酸以抑制K(Ca)和Cl(Ca)电流时，SHR和DOCA高血压细胞的K(v)电流明显小于对照。最后，与对照细胞相比，SHR和DOCA高血压细胞的基础和血管紧张素II刺激的细胞内游离[Ca2+]峰值更高。这些结果表明，高血压大鼠肾叶间动脉的膜电位以及K(Ca)和K(v)通道的活性发生了改变，可能在生理和病理生理条件下肾血流的调节中发挥作用。
