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

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

Treatments

Strain

n

-logEC50

(M)

Emax

(%)

Hill slope

n

-logEC50

(M) a

Emax

(%)

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)

  1. 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.
  2. C57, C57BL/6J mice; Emax, maximum relaxation response where 100% is complete reversal of contraction; PAR2-/-, protease-activated receptor 2 gene knockout mice.