High-Dose Estradiol-Replacement Therapy Enhances the Renal Vascular Response to Angiotensin II via an AT₂-Receptor Dependent Mechanism

Table 1

Hemodynamic variables before vehicle or PD123319 administration and body, uterus, and kidney weights at postmortem.

Group	BW; g	UW; mg	KW; g	MAP; mmHg	RPP; mmHg	RBF; mL/min/g KW	RVR; mmHg/mL/min/g KW
OV	192 ± 8	35 ± 4	0.66 ± 0.03	103 ± 6	94 ± 6	2.7 ± 0.3	35 ± 3
OV + PD	203 ± 11	45 ± 12	0.70 ± 0.03	106 ± 2	99 ± 2	2.9 ± 0.4	37 ± 6
OV + E	185 ± 9	202 ± 19	0.62 ± 0.03	100 ± 4	91.7 ± 3	2.1 ± 0.1	44 ± 1
OV + E + PD	183 ± 6	201 ± 26	0.72 ± 0.04	109 ± 5	102 ± 4	2.5 ± 0.2	44 ± 2
Sham	190 ± 4	107 ± 7		—	—	—	—
	0.4	<0.0001	0.2	0.5	0.3	0.2	0.3

Data are presented as mean ± SEM of . The values were derived from one-way ANOVA. Specific contrasts were generated by Tukey’s post hoc comparisons. for comparison with ovariectomized rats treated with the vehicles for estrogen and PD123319. for comparison with all ovariectomized rats. OV: ovariectomized, E: estradiol, PD: PD123319, BW: body weight, UW: uterus weight, KW: kidney weight, MAP: mean arterial pressure, RPP: renal perfusion pressure, RBF: renal blood flow per gram kidney weight, and RVR: renal vascular resistance.