Estrogen restores role of basal nitric oxide in control of vascular tone in rats with chronic heart failure.

Abstract

This study examined the cardiovascular effects of 17beta-estradiol in ovariectomized rats with heart failure. Two groups (50-60 days old) were implanted with 60-day-release pellets containing 17beta-estradiol (25 microg/day) or vehicle at 7 days before ligation of the left coronary 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 pressure (MAP, -24 +/- 6 mmHg), cardiac output (-27 +/- 4 ml/min), left ventricular (LV) end-systolic pressure (-29 +/- 8 mmHg), depressor responses to ACh (-6 +/- 4 mmHg at 7.2 microg/kg) and sodium nitroprusside (SNP, -22 +/- 6 mmHg at 9 microg/kg), and pressor responses to NG-nitro-L-arginine methyl ester (L-NAME, -14 +/- 6 mmHg at 8 mg/kg) and increased LV end-diastolic pressure (LVEDP, 10.3 +/- 0.8 mmHg) but no change in total peripheral resistance (TPR). Treatment of ligated rats with 17beta-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 responses to L-NAME (14 +/- 3 mmHg) but did not alter other variables. Therefore, 17beta-estradiol reduces preload and afterload and restores the vasodilator role of basal nitric oxide in ovariectomized rats with chronic heart failure.