Sympathetic vasomotor over activation is recognized today as an important determinant of blood pressure levels in primary and secondary arterial hypertension, however, however, the mechanisms underlying sympathetic hypertonia, how it is established and what is its participation not only in triggering but also in the maintenance of arterial hypertension are not yet fully understood. We have investigated in an experimental secondary hypertension model, the Goldblatt model (2K1C) how the central nervous system controls the sympathetic vasomotor activity in the Goldblatt hypertension. The increase in the activity of brain nuclei such as the paraventricular nucleus of the hypothalamus (PVN), the rostroventrolateral region of the medula oblongata (RVLM) has been shown by us and by others to be essential for sympathetic vasomotor hyperactivity in renovascular hypertension. The role of reactive oxygen species in these nuclei is fundamental to the process of increasing sympathetic vasomotor activity. Both the PVN and the RVLM region project monosynaptically to the intermediate-lateral column (IML) of the spinal cord, a site that contains the pre-ganglionic neurons of the sympathetic. We recently described that in this region there is an increase in the expression of angiotensin II AT1 receptors and that losartan, intrathecal injected, produces a reduction in sympathetic activity only in the 2K1C model. We do not, however, have information about the action of reactive oxygen species on the activity of sympathetic pre-ganglionic neurons in renovascular hypertension, which is, therefore, the object of this research project.
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