Table 1.

Effects of heparin on IP₃-evoked Ca²⁺ release and IP₃ binding

		Functional analysis		aBinding	pEC50(IP3)-pKD(heparin)
		IP3 or AdA	heparin	heparin
		pEC50	pKD	pKD
IP3R1	IP3	7.47 ± 0.02	5.39 ± 0.00	4.66	2.08 ± 0.02
IP3R1	AdA	8.35 ± 0.03	5.16 ± 0.05	–	–
IP3R2	IP3	6.82 ± 0.04	4.66 ± 0.07	4.62	2.16 ± 0.09*
IP3R3	IP3	6.66 ± 0.07	5.55 ± 0.09	5.34	1.11 ± 0.08*
IP3R3	AdA	7.71 ± 0.01	5.68 ± 0.04	–	–

From experiments similar to those shown in Figures 1 and 2, AdA or IP₃-evoked Ca²⁺ release and their sensitivity to heparin were used to determine pEC₅₀ (as M) and pK_D (as g mL⁻¹) for DT40 cells expressing IP₃R1, IP₃R2 or IP₃R3. Results are means ± SEM from three independent experiments (six for IP₃R3).

^aThe affinities for heparin determined from equilibrium-competition binding with ³H-IP₃ to Sf9 membranes expressing IP₃R1-3 are reproduced from (Nerou et al., 2001). The batch of heparin used for those binding studies was different from that used for the work reported here. The final column (derived from the results shown in Figures 1B,C and 2A–D) shows paired comparisons of pEC₅₀(IP₃) – pK_D(heparin) as a means of reporting the relative effectiveness with which heparin might be expected to block IP₃-evoked Ca²⁺ release via different IP₃R subtypes. The results suggest that IP₃R3 is likely to be substantially more susceptible to inhibition than IP₃R1 or IP₃R2.

^*Denotes a value significantly different from IP₃R1 in the final column (P < 0.05).