Altered frequency characteristics of sympathetic nerve activity after sustained elevation in arterial pressure.

We tested the hypothesis that sustained elevation in mean arterial pressure (MAP) alters the frequency-domain characteristics of efferent sympathetic nerve discharge (SND) after the return of MAP to control levels. Renal, lumbar, and splanchnic SND were recorded before, during, and after a 30-min increase in MAP produced by phenylephrine (PE) infusion in α-chloralose-anesthetized, spontaneously hypertensive (SH) rats. The following observations were made. 1) The basic cardiac-locked pattern of renal, lumbar, and splanchnic SND bursts was altered after sustained elevation in MAP, demonstrating prolonged effects on the neural circuits involved in entraining efferent SND to the cardiac cycle. Importantly, discharge bursts in afferent baroreceptor nerve activity remained pulse-synchronous after sustained increases in arterial pressure. 2) The frequency-domain relationships between the activity in sympathetic nerve pairs were altered after sustained elevation in MAP, suggesting a transformation from a system of tightly coupled neural circuits to one of multiple generators exerting selective control over SND. 3) The most prominent reduction in SND power after sustained elevation in MAP occurred in the frequency band containing the cardiac cycle, indicating that the prolonged suppression of SND after sustained increases in arterial pressure is due primarily to the selective inhibition of cardiac-related SND bursts. We conclude that sustained elevation in MAP profoundly affects the neural circuits responsible for the frequency components of basal SND in SH rats.