| Grant number: | 13/22522-9 |
| Support Opportunities: | Regular Research Grants |
| Start date: | September 01, 2014 |
| End date: | August 31, 2017 |
| Field of knowledge: | Biological Sciences - Physiology - Physiology of Organs and Systems |
| Principal Investigator: | Ruy Ribeiro de Campos Junior |
| Grantee: | Ruy Ribeiro de Campos Junior |
| Host Institution: | Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil |
| City of the host institution: | São Paulo |
| Associated researchers: | Adriana Castello Costa Girardi ; Alex Yuri Simões Sato ; Cassia Marta de Toledo Bergamaschi ; Guiomar Nascimento Gomes |
Abstract
The renovascular hypertension dependent of angiotensin II (Ang II) is characterized by sympathetic overactivity and, therefore, has a strong neurogenic component. Previous studies from our laboratory showed that in the 2 kidney-one clip model (2K-1C) in rats the increased renal sympathetic nerve activity (RSNA) contributes for the development of hypertension and there is an increase in the expression of AT1 Ang II receptor in brain regions involved with the cardiovascular control as well as in the ischemic kidney. Such data suggest that there is an interaction between central and renal mechanisms related to the Ang II actions leading to Sympathoexcitation in renovascular hypertension. Thus, our hypothesis is that the sympathetic overactivity in renovascular hypertension leads to changes in the AT1 and AT2 Ang II receptors expression in a differential way in the ischemic and contralateral kidney of 2K-1C rats, leading therefore, morphological and physiological renal changes leading to increase in blood pressure. The major aim of the present project will evaluate the effects of renal denervation of ischemic kidney, that releases renin, from hypertensive rats leads to changes in the expression of Ang II receptors (AT1 and AT2) in the cortex and medulla of ischemic and contralateral kidney. Furthermore, considering that this is a model with a strong neurogenic component, the expression of such receptors will be evaluated in the regions of central nervous system related to cardiovascular regulation, such as, RVLM and PVN, that are involved in the control of sympathetic vasomotor activity and RSNA. For comparison, in another series of experiments the rats will be treated with Losartan, an AT1 receptor antagonist (30 mg/Kg/day), or a non-specific antihypertensive drug, hidralazyn (25 mg/Kg/day), to differentiate the changes related to fall in blood pressure and reduction in RSNA. The data, altogether will improve our understanding of the cross-talk between the central nervous system and the kidneys regarding the hypertension. (AU)
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