Ganfornina M D, López-Barneo J
Departamento de Fisiología y Biofísica, Facultad de Medicina, Universidad de Sevilla, Spain.
Proc Natl Acad Sci U S A. 1991 Apr 1;88(7):2927-30. doi: 10.1073/pnas.88.7.2927.
Type I cells of the carotid body are known to participate in the detection of O2 tension in arterial blood but the primary chemotransduction mechanisms are not well understood. Here we report the existence in excised membrane patches of type I cells of a single K+ channel type modulated by changes in PO2. Open probability of the O2-sensitive K+ channel reversibly decreased by at least 50% on exposure to hypoxia but single-channel conductance (approximately 20 pS) was unaltered. In the range between 70 and 150 mmHg (1 mmHg = 133 Pa) the decrease of single-channel open probability was proportional to the PO2 measured in the vicinity of the membrane patch. The inhibition of K+ channel activity by low PO2 was independent of the presence of non-hydrolyzable guanine triphosphate analogues at the internal face of the membrane. The results indicate that the O2 sensor of type I cells is in the plasma membrane and suggest that environmental O2 interacts directly with the K+ channels.
已知颈动脉体的I型细胞参与动脉血中氧分压的检测，但主要的化学转导机制尚不清楚。在此我们报告，在I型细胞的离体膜片中存在一种受氧分压变化调节的单一类型钾通道。暴露于低氧环境时，氧敏感钾通道的开放概率可逆性降低至少50%，但单通道电导（约20 pS）未改变。在70至150 mmHg（1 mmHg = 133 Pa）范围内，单通道开放概率的降低与膜片附近测得的氧分压成正比。低氧对钾通道活性的抑制与膜内表面不可水解的鸟嘌呤三磷酸类似物的存在无关。结果表明，I型细胞的氧感受器位于质膜上，并提示环境氧直接与钾通道相互作用。
