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Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas 66506
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
-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.
phenylephrine; spontaneously hypertensive rats; aortic depressor nerve activity; autospectral analysis
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