The long term objective of this research is to determine how the central nervous system increases sympathetic nerve discharge (SND) and formulates differential patterns of sympathetic outflow during various physiological states including the defense reaction, hemorrhagic shock and somatic afferent stimulation. Most of the power in SND is contained between 1 and 10 Hz. This low frequency rhythm is a characteristic feature of those central circuits involved in generation of basal SND. However, the influence of acute stress on the frequency components in SND and the frequency-domain relationships between the discharges in different sympathetic nerves is not known. The studies described in this proposal will determine if acute physical stress (e.g., hypercapnia, hypoxemia, heating, hemorrhage, somatic afferent stimulation, hypertonic saline infusion and the defense reaction): 1) produces an upward shift in the frequency of the sympathetic rhythm; 2) uncouples the discharges of sympathetic nerve pairs; 3) alters the frequency components and frequency-domain relationships between the discharges in different sympathetic nerves in conscious rats; 4) produces an increased state of excitability within the central circuits responsible for generation of SND; and 5) changes the frequency-domain relationships between rostral ventral lateral medullary neurons and SND. Multi fiber recordings of postganglionic sympathetic nerve pairs are used to determine the influence of acute stress on the frequency components in SND. Single- unit recordings are used to determine if the spontaneous activity of medullary neurons is changed during periods of acute stress. Auto spectral and coherence analyses are used to quantitate the frequency components in SND. Peripheral blood flows are recorded to provide information concerning the functional significance of alterations in the frequency-domain characteristics of SND. The immunocytochemical labelling of c-fos containing neurons is completed to identify central nervous system neurons which are activated by acute physical stress. It is well established that the sympathetic nervous system is involved in the pathogenesis of several forms of hypertension. The proposed studies will provide important new information concerning how the functional relationships between the central circuits involved in generation of SND are recorded during periods of acute physical stress. Further understanding of the organization of sympathetic central circuits may provide information concerning the role of the central nervous system in the development and maintenance of hypertension.
