The Proatherogenic Effect of Chronic Nitric Oxide Synthesis Inhibition in ApoE-Null Mice Is Dependent on the Presence of PPARα

Table 1

Animals weights and systolic blood pressure at baseline and following treatment and biochemical measurements at the end of the study. The number of mice in each subgroup is shown in parentheses.

Parameter	ApoE-null; males; 𝑛=26	ApoE-null; females; 𝑛=23	DKO; males; 𝑛=25	DKO; females; 𝑛=19	P
Baseline weight (g)	23.6 ± 0.6	19.0 ± 0.6	26.3 ± 0.7	21.4 ± 0.7	<0.01 (males); 0.01 (females)
End weight control (g)	26.2 ± 0.8 (13)	21.6 ± 0.7 (9)	36.3 ± 1.6 (15)	29.0 ± 1.4 (10)	<0.0001*
End weight L-NAME (g)	27.7 ± 1.1 (13)	22.1 ± 0.5 (14)	32.8 ± 1.6 (10)	26.4 ± 0.6 (9)	<0.0001*
Baseline blood pressure^† (mm Hg)	106.6 ± 1.7		101.0 ± 2.1		NS^†
End blood pressure control (mm Hg)	104.8 ± 2.9		104.1 ± 4.2		NS
End blood pressure L-NAME (mm Hg)	101.7 ± 1.7		102.9 ± 2.5		NS^†
Cholesterol control (mg/dL)^‡	737 ± 93§		1451 ± 147		0.001
Cholesterol L-NAME (mg/dL)	1021 ± 63		1026 ± 102		NS
Triglycerides control (mg/dL)	86.1 ± 6.4§		288.7 ± 47.9		<0.0001
Triglycerides L-NAME (mg/dL)	132.4 ± 14.5		260.5 ± 36.5		<0.0005

∗For gender-specific comparisons.
^†Blood pressure data are presented for males and females together as there were no differences between sexes. There were no differences between lines, treatment groups, or the time point at which blood pressure was measured.
^‡Biochemical data are presented for males and females together as there were no differences between sexes in neither line.
§P < 0.05 for comparison between ApoE-null control and ApoE-null with L-NAME.