Carotid baroreceptor stimulation has been clinically explored for antihypertensive benefits but aortic baroreceptor modulation remains untouched for clinical translation. Published studies use large current/voltage amplitudes (10V), longer pulse widths (2 ms) or ultra-high frequencies (70-100 Hz). These are energy inefficient neuromodulation methods. Our main goal was to identity optimal nerve stimulation parameters that would provide a sustained drop in mean arterial pressure (MAP) of ~30 mmHg. We stimulated aortic depressor nerve (ADN) in spontaneously hypertensive rats (SHR,
n
=4) at low ranges of frequencies, pulse amplitudes and pulse widths. Under urethane anesthesia, left ADN was stimulated for 20 seconds at varying frequencies (1, 2.5 and 5 Hz) and pulse amplitudes (0.2, 0.4 and 0.6 mA) at 0.1, 0.2 or 0.5 ms pulse width. A frequency-dependent depressor response was seen at all pulse amplitudes and widths used. Lower pulse amplitudes (0.2 mA) produced ~18 mmHg MAP drop at all pulse widths tested. Higher pulse amplitude (0.4 and 0.6 mA) produced similar drop in MAP of ~34 mmHg. The return to baseline values was relatively prolonged with higher charge injection with 32 seconds at 0.2 mA (0.1 or 0.2 ms at 5 Hz, maximum effect size: -18 mmHg) versus 42 seconds at 0.4 or 0.6 mA (0.1, 0.2 or 0.5 ms at 5 Hz, maximum effect size: -34 mmHg). There was no added benefit of pulse amplitudes beyond 0.4 mA. We conclude that low intensity stimulation is an effective alternate way to neuromodulation of the ADN. This will enable low energy consumption for neuromodulation. Future studies will study impact of these parameters in conscious SHR rats.