Protection of protease-activated receptor 2 mediated vasodilatation against angiotensin II-induced vascular dysfunction in mice

Table 3 Nitroprusside concentration-response curves of mesenteric arteries from saline- and angiotensin II-treated mice.

Treatments	Strain	n	-logEC₅₀ (M)	E_max (%)	Hill slope	n	-logEC₅₀ (M) ^a	E_max (%)	Hill slope
		Saline				Angiotensin II
Control	C57	27	7.7(0.1)	95(1)	0.9(0.1)	36	7.4(0.1)^b	94(2)	1.2(0.1)
control ^c	PAR2^-/-	13	7.6(0.2)	96(1)	0.9(0.3)	10	7.7(0.2)	96(1)	1.0(0.3)
NS398	C57	7	7.8(0.3)	94(2)	1.3(0.4)	11	7.3(0.2)	95(1)	1.7(0.4)
FR122047	C57	9	7.7(0.2)	95(3)	1.1(0.2)	11	7.2(0.2)	94(2)	1.3(0.3)
AH6809 + L798106 + L161982	C57	5	7.4(0.2)	95(2)	1.3(0.5)	4	7.9(0.1)	96(1)	2.2(1.0)
CAY10441	C57	6	7.9(0.2)	96(1)	1.2(0.4)	5	7.4(0.3)	96(1)	1.7(0.8)

Values are mean (SE), n = number of mice. Variables were determined by curve fitting data points from cumulative drug concentration-responses relationships to a four parameter logistic equation. Treatments of arteries included antagonists of COX-1 (1 μM FR122047), COX-2 (3 μM NS398), prostaglandin E₂ receptors (1 μM AH6809, 1 μM L798106, 0.1 μM L161982), prostaglandin I₂ receptor (0.1 μM CAY10441). Comparisons were made by two-way ANOVA (pump × artery treatments) [^aP < 0.05, effect of pump (saline vs. angiotensin II)] followed by Bonferroni post hoc tests: ^bP < 0.05, control compared to saline pump treatment; ^cdata of control arteries from PAR2^-/- were included as a treatment factor for analyses.
C57, C57BL/6J mice; E_max, maximum relaxation response where 100% is complete reversal of contraction; PAR2^-/-, protease-activated receptor 2 gene knockout mice.