{'fraction_non_alphanumeric': 0.058609958506224066, 'fraction_numerical': 0.01867219917012448, 'mean_word_length': 5.473154362416107, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Endothelial and neuronal nitric oxide synthases variably modulate the oestrogen‐mediated control of blood pressure and cardiovascular autonomic control

We have shown previously that long‐term oestrogen (E2) replacement lowers blood pressure (BP) and improves cardiovascular autonomic control in ovariectomized (OVX) rats. In the present study, we investigated whether constitutive and/or inducible (i) nitric oxide synthase (NOS) modulate these E2 effects. We evaluated changes in BP, myocardial contractility index (dP/dtmax) and power spectral indices of haemodynamic variability following selective inhibition of endothelial (e) NOS with N5‐(1‐iminoethyl)‐ l‐ornithine (l‐NIO), neuronal (n) NOS with Nω‐propyl‐l‐arginine (NPLA) or iNOS with 1400W in telemetered OVX rats treated for 16 weeks with (OVXE2) or without (control; OVXC) E2. The 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. Inhibition of eNOS (l‐NIO; 20 mg/kg, i.p.) elicited a shorter‐lived pressor response in OVXE2 than OVXC, rats along with reductions in dP/dtmax and increases in the spectral index of spontaneous baroreflex sensitivity (index α). Treatment with 1 mg/kg, i.p., NPLA reduced BP and increased the IBILF/HF ratio in OVXE2 but not OVXC rats. The iNOS inhibitor 1400W (5 mg/kg, i.p.) caused no haemodynamic changes in OVXC or OVXE2 rats. Overall, constitutive NOS isoforms exert restraining tonic modulatory BP effects that encompass eNOS‐mediated reductions and nNOS‐mediated elevations in BP in OVXE2 rats. Baroreflex facilitation and dP/dtmax reductions may account for the shorter pressor action of l‐NIO in E2‐treated, compared with untreated, OVX rats.