| Grant number: | 16/22069-0 |
| Support Opportunities: | Regular Research Grants |
| Start date: | February 01, 2017 |
| End date: | January 31, 2019 |
| Field of knowledge: | Health Sciences - Physical Education |
| Principal Investigator: | Thiago dos Santos Moreira |
| Grantee: | Thiago dos Santos Moreira |
| Host Institution: | Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil |
| City of the host institution: | São Paulo |
Abstract
The pathophysiology of systemic arterial hypertension is complex and in general poorly understood, but over the last 3 decades studies in animal models and patients with hypertension have provided significant evidence that activation of the sympathetic nervous system is linked to the development and maintenance of the condition. Vasomotor and cardiac activities of spinal sympathetic preganglionic neurons depend on tonic descending excitatory drive generated by sympathoexcitatory (presympathetic) neuronal networks residing in the hypothalamus and the brainstem: the rostral ventrolateral medulla (RVLM), rostral ventromedial and midline medulla, the A5 cell group of the pons, and the paraventricular hypothalamic nucleus. Bulbospinal neurons of the RVLM which belong to the catecholaminergic C1 group are believed to be of a prime importance for the maintenance of vasomotor sympathetic tone.One of the potential mechanisms which may be responsible for sympathetic activation in hypertension is based on the operation of a so-called Cushing response characterized by a triad of high blood pressure, irregular breathing, and bradycardia. Although originally described as an autoresuscitation mechanism recruited under extreme pathological conditions such as brain ischemia, it is currently viewed as a physiological compensatory response to compromised brain perfusion or brain hypoxia. Brainstem vasculature of patients with hypertension and of animal models of hypertension (eg, spontaneously hypertensive rat [SHR]) is considerably narrower (compared with the respective normotensive counterparts), resulting in high cerebral artery resistance. This is not a consequence of hypertension as it occurs prior to its development, at least in the SHR. Thus, the neuronal sympathoexcitatory networks that control the arterial blood pressure have been suggested to be hypoperfused/hypoxic. By increasing systemic arterial blood pressure in response to compromised brainstem perfusion, the Cushing mechanism would be expected to produce changes in the circulatory system to preserve oxygen delivery and maintain brain oxygenation at the expense of systemic hypertensionThe mechanisms underlying sympathetic activation associated with compromised brain tissue perfusion and hypoxia remain unknown. This project was designed to test the hypothesis that brainstem hypoperfused is associated with the pathogenesis of systemic arterial hypertension (AU)
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