Figure 4. Blockade of intracellular Ca²⁺ responses to acidic hypercapnia by 2 m.

mNi²⁺A, acidic hypercapnia (10% CO₂, pH 7.1) elicited a rise in [Ca²⁺]_i in a carotid body (CB) type I cell that was reversibly blocked by the non-specific voltage-gated Ca²⁺ channel antagonist, 2 mm Ni²⁺. The same protocol was applied in B, although in this case the CB type I cells exhibited spontaneous activity before and especially after washout of the stimulus; 2 mm Ni²⁺ reversibly blocked the spontaneous activity as well as the response to acidic hypercapnia. In C, an aortic body (AB) type I cell with spontaneous activity responded to acidic hypercapnia, and this response was blocked by 2 mm Ni²⁺; note that application of Ni²⁺ immediately caused a reduction in the baseline [Ca²⁺]_i, as indicated by the hatched lines. Although the effect of acidic hypercapnia was poorly reversible, there was still a detectable response to high K⁺. Cumulative data for all 10% CO₂/H⁺-responsive CB and AB type I cells exposed to this protocol are illustrated in D and E.