This application is based on microdialysis experiments in which NE release was monitored simultaneously from paraventricular (PVN) and posterior nucleus (PH) of the hypothalamus in the freely moving rats before, during and after imposition of a quantifiable, painless, environmental stressor, """"""""shaker stress"""""""". Shaker stress cause an immediate pressor effect, heart rate change and increases the release of NE at both hypothalamic sites; after stress mean arterial pressure (MAP) and heart rate (HR) return to control levels but enhanced NE release persists, longer in PH than PVN.
Specific aims are focused to test the hypotheses that cardiovascular changes are, in part or totally, independent of hypothalamic NE release during shaker stress and that the pressor response attenuates the hypothalamic NE release. Spontaneously hypertensive rats (SHR) have an exaggerated pressor response to shaker stress. We hypothesize that SHR have a greater and/or different pattern of hypothalamic NE release than controls and that adrenoceptor modulation of release is different in SHR than controls. Finally the mechanism of post-stress, enhanced NE release in PVN and PH will be determined. Protocols require continuous measurement of MAP and HR and the simultaneous collection of 5 minute dialysate samples, obtained with 1 mm long microdialysis probes in PVN and PH, from freely moving rats. Extracellular NE will be measured by sensitive radioenzymatic assay. These studies will provide new data on central integrative mechanisms of noradrenergic and cardiovascular activity in hypertension and during stress.
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