The carotid body's glomus cells are the primary sensors of hypoxia in mammals. Previous studies suggested that the glomus cells' hypoxia sensitivity is mediated by lactate in mice. This molecule increases the intracellular [Ca²⁺] and induces exocytosis in glomus cells, activating the carotid sinus nerve (the axons of chemoreceptive petrosal neurons). On the other hand, how lactate affects the activity of carotid body of rats is still unknown. We hypothesized that lactate activates the carotid body of rats. In Wistar rats, we measured the changes in the electrical properties of isolated glomus cells and petrosal chemoreceptive neurons in in situ preparations in response to different concentrations of lactate. Superfusion of both physiological and supraphysiological concentrations of lactate did not affect the membrane conductance and potential of glomus cells. Moreover, lactate injected into the carotid body did not activate the anatomically and physiologically identified chemoreceptive petrosal neurons. We conclude that the carotid body of Wistar rats is not sensitive to lactate.

颈动脉体的血管球细胞是哺乳动物缺氧的主要传感器。先前的研究表明，球状细胞的缺氧敏感性是由小鼠的乳酸介导的。该分子增加细胞内 [Ca ²⁺ ] 并诱导血管球细胞的胞吐作用，激活颈动脉窦神经（化学感受性岩骨神经元的轴突）。另一方面，乳酸对大鼠颈动脉体活动的影响尚不清楚。我们假设乳酸会激活大鼠的颈动脉体。在 Wistar 大鼠中，我们原位测量了离体球细胞和岩骨化学感受神经元的电特性变化对不同浓度乳酸的反应。乳酸的生理和超生理浓度的灌注不影响球细胞的膜电导和电位。此外，注射到颈动脉体中的乳酸不会激活解剖学和生理学上鉴定的化学感受性岩骨神经元。我们得出结论，Wistar 大鼠的颈动脉体对乳酸不敏感。