Chronic inhibition of endothelial nitric oxide synthase activity in nucleus tractus solitarii enhances baroreceptor reflex in conscious rats

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Abstract

In acute experiments, we demonstrated previously that nitric oxide (NO) donors exogenously applied to the nucleus tractus solitarii (NTS) depressed the baroreceptor cardiac reflex. In this study, we determined a role for endogenous endothelial nitric oxide synthase (eNOS) activity in the NTS for chronically regulating baroreceptor reflex function in conscious rats. A recombinant adenoviral vector directing expression of a truncated form of eNOS was microinjected bilaterally into the NTS to inhibit endogenous eNOS activity. Arterial pressure was monitored continuously using radio-telemetry in freely moving animals and spontaneous baroreceptor reflex gain (sBRG) determined by a time-series method. sBRG showed a gradual increase from day 7 to 21 after gene transfer and the value at day 21 (1.68 +/- 0.20 ms mmHg(-1), n = 6) was significantly higher than that before gene transfer (1.13 +/- 0.09 ms mmHg(-1), P < 0.001). This value was also significantly higher than that in rats in which enhanced green fluorescent protein (eGFP) was expressed in the NTS (1.04 +/- 0.21 ms mmHg(-1); n = 6, P < 0.01) and saline-treated groups (1.12 +/- 0.15 ms mmHg(-1); n = 4, P < 0.05), which did not change from control levels. In addition, heart rate decreased from 336 +/- 6 to 318 +/- 8 b.p.m. (P < 0.05) 21 days after gene transfer. This value was also significantly lower than that in control groups (eGFP: 348 +/- 9 b.p.m., n = 6, P < 0.01; saline: 347 +/- 5 b.p.m., n = 4, P < 0.05). Gene transfer did not affect arterial pressure. These findings suggest that in the conscious rat eNOS is constitutively active within the NTS and is a factor regulating baroreceptor reflex gain and heart rate.

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