We have previously shown that long‐term estrogen (E2) replacement lowers blood pressure (BP) and improves the cardiovascular autonomic control in ovariectomized (OVX) rats. In this study, we investigated whether constitutive and/or inducible nitric oxide synthase (NOS) modulate these E2 effects.We evaluated changes in BP, myocardial contractility index (dP/dtmax), and power spectral indices of hemodynamic variability following selective inhibition of eNOS [N5‐(1‐iminoethyl)‐L‐ornithine; L‐NIO], nNOS (Nω‐propyl‐L‐arginine; NPLA), or iNOS (1400W) in telemetered OVX rats treated for 16 weeks with (OVXE2) or without (control, OVXC) E2.OVXE2 rats exhibited: (i) reduced BP, and increased dP/dtmax, (ii) cardiac parasympathetic dominance as reflected by the reduced low‐frequency (LF, 0.25‐0.75 Hz)/high‐frequency (HF, 0.75‐3 Hz) ratio of interbeat intervals (IBILF/HF), and (iii) reduced LF oscillations of systolic BP, suggesting a reduced vasomotor sympathetic tone.eNOS inhibition (L‐NIO, 20 mg/kg i.p.) elicited a shorter‐lived pressor response in OVXE2, than in OVXC, rats along with reductions in dP/dtmax and increases in the spectral index of spontaneous baroreflex sensitivity (index α). NPLA (1 mg/kg i.p.) reduced BP and increased IBILF/HF ratio in OVXE2, but not OVXC rats. The iNOS inhibitor 1400W (5 mg/kg i.p.) caused no hemodynamic changes in OVXC or OVXE2 rats.Overall, constitutive NOS isoforms exert restraining tonic modulatory BP effects, which encompass eNOS‐mediated reduction and nNOS‐mediated elevation in BP in OVXE2 rats. Baroreflex facilitation, and dP/dtmax reductions might account for the shorter pressor action of L‐NIO in E2‐treated, compared with untreated, OVX rats. This article is protected by copyright. All rights reserved.