Arterial hypertension (AH) is a highly prevalent syndrome and the control of blood pressure in some patients is still a challenge. Several mechanisms are involved in the pathophysiology of AH, such as the renin-angiotensin-aldosterone system, hydroelectrolytic imbalance, renal dysfunction and increased activity of the sympathetic nervous system (SNS). The SNS influences renal function by controlling renin secretion, renal blood flow and sodium excretion. Moreover, the kidney is richly innervated by sensory afferent fibers that may interact with the SNS. Simultaneously measurement of the afferent renal nerve activity (ARNA) and renal sympathetic nerve renal activity (rSNA) suggests that increases in the ARNA leads to decreases in the rSNA, which is known as reno-renal inibitory reflex. This reflex is likely to be mediated by interactions between regulatory nuclei of the cardiovascular system in the central nervous system. Furthermore, evidences suggest that increased ARNA contributes to increased rSNA in AH. The failure of the reno-renal inibitory reflex has been implicated in the renal sympathoexcitation in the 2 kidney - 1 clip (2K1C) model of AH. Although the brain structures activated by afferent renal fibers stimulation have been identified anatomically, the activated neurons in this structures have not been characterized. Because catecholaminergic neurons play an important role in the regulation of the cardiovascular system, this project aims to investigate whether the neurons activated by increased ARNA are tyrosine hydroxylase-positive in normotensive and 2K1C hypertensive Wistar rats.
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