ESTROGEN RESTORES ROLE OF BASAL NITRIC-OXIDE IN CONTROL OF VASCULAR TONE IN RATS WITH CHRONIC HEART-FAILURE

This study examined the cardiovascular effects of 17 beta-estradiol in ovariectomized rats with heart failure. Two groups (50-60 days old) w ere implanted with 60-day-release pellets containing 17 beta-estradiol (25 mu g/day) or vehicle at 7 days before Ligation of the left corona ry artery. Another group was sham operated and given vehicle pellets. After 7 wk, they were studied under pentobarbital anesthesia. Relative to sham-operated rats, ligated rats had reduced mean arterial pressur e (MAP, -24 +/- 6 mmHg), cardiac output (-27 +/- 4 ml/min), left ventr icular (LV) end-systolic pressure (-29 +/- 8 mmHg), depressor response s to ACh (-6 +/- 4 mmHg at 7.2 mu g/kg) and sodium nitroprusside (SNP, -22 +/- 6 mmHg at 9 mu g/kg), and presser responses to NG-nitro-L-arg inine methyl ester (L-NAME, -14 +/- 6 mmHg at 8 mg/kg) and increased L V end-diastolic pressure (LVEDP, 10.3 +/- 0.8 mmHg) but no change in t otal peripheral resistance (TPR). Treatment of ligated rats with 17 be ta-estradiol reduced TPR (-0.19 +/- 0.06 mmHg.min.ml(-1)), LVEDP (-3.6 +/- 1 mmHg), and responses to ACh (-16 +/- 4 mmHg) and augmented resp onses to L-NAME (14 +/- 3 mmHg) but did not alter other variables. The refore, 17 beta-estradiol reduces preload and afterload and restores t he vasodilator role of basal nitric oxide in ovariectomized rats with chronic heart failure.