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Effects of cross-fostering on normotensive and hypertensive rats: evaluation of heart collagen deposition

Grant number: 19/19125-4
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Effective date (Start): April 01, 2020
Effective date (End): March 31, 2021
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal Investigator:Luciana Venturini Rossoni
Grantee:Mariana Moreira Felix de Oliveira
Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil


Hypertension is a disease characterized by a chronic increase in arterial, systolic and/or diastolic, blood pressure (BP), being a major risk factor for other cardiovascular, cerebrovascular and renal diseases. It has become one of the major public health concerns nowadays due to its high morbidity and mortality. Several hypertension risk factors have already been described, such as overweight and obesity, physical inactivity, poor diet, genetic components, and maternal-fetal and postnatal environments, such as breast milk composition. In turn, the influence of breast milk on offspring is evaluated by a technique called cross-fostering, in which, in the case of hypertension, littler of normotensive rats (Wistar) and hypertensive rats (spontaneously hypertensive rats, SHR) are cross-fostered. Some studies, including preliminary results from our group, have already demonstrated that SHR breastfed by normotensive mothers have delayed and/or reduced BP values when compared to those observed in SHRs breastfed by their hypertensive biological mothers. with no change in heart rate values. On the other hand, normotensive rats breastfed by hypertensive mothers do not show changes in BP values, while having tachycardia. It is well known that chronic BP overload (afterload), as well as sympathetic nervous system activation, causes cardiac remodeling, in which structural and molecular adjustments occur. Our preliminary results showed that cross-fostering wasn't able to modify the cardiomyocyte hypertrophy from the left or right ventricle observed in SHR, but induced it in Wistar rats. It is known that in the hypertensive process, in addition to cardiomyocyte hypertrophy, increased collagen deposition is observed, which contributes to ventricular stiffness, an important step for future diastolic heart dysfunction. Within this context, the present project aims to evaluate ventricular collagen deposition and potential signaling pathways involved in this process in SHR and Wistar rats that are cross-fostered. (AU)

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