TABLE 2.

Sensitivity (EC₅₀) and magnitude (Rmax) of vascular responses to ET-1 and ACh in the absence or presence of ET receptor antagonists in basilar arteries of control Wistar and diabetic GK rats.

	Wistar + Vehicle (n=8)	Wistar + Atrasentan (n=10)	Wistar + A-192621 15 mg/kg (n=3)	Wistar + A-192621 30 mg/kg (n=5)
ET-1 constriction
EC50 (nM)	11.3 ± 1.7	0.6 ± 0.2a,*	4.1 ± 1.8	32 ± 2.1a,b
Rmax (%baseline)	99 ± 15	159 ± 28	139 ± 29a	56 ± 16
Ach relaxation
EC50 (nM)	4.7 ± 1.5	8.1 ± 1.8	15.9 ± 4.0	2.0 ± 1.6
Rmax (% 5HT)	56 ± 5	46 ± 8	53 ± 5	90 ± 8a,*
	GK+ Vehicle (n=6)	GK + Atrasentan (n=6)	GK + A-192621 15 mg/kg (n=3)	GK + A-192621 30 mg/kg (n=6)
ET-1 constriction
EC50 (nM)	2.8 ± 1.6c	20 ± 2.2 c,d,*	2.2± 3.6	2.6 ± 3.1
Rmax (% baseline)	115 ± 22	128 ± 14	203 ± 43e	95 ± 25f
Ach relaxation
EC50 (nM)	2.4 ± 2.0	3.8 ± 1.4	3.6 ± 4.3	4.3 ± 4.6
Rmax (% 5HT)	26 ± 4c	64 ± 3c	27 ± 7c	−2 ± 14d,g,*

^ap<0.01 vs vehicle Wistar

^bp<0.001 vs Atrasentan or A-192621 15 mg/kg Wistar

^cp<0.01 vs vehicle Wistar

^dp<0.001 vs GK treatment groups

^ep<0.05 vs vehicle GK

^fp<0.05 vs A-192621 15 mg/kg GK

^hp<0.001 vs Wistar

^*p<0.0001-disease-treatment interaction in Wistar vs GK rats.