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Isoforms of angiotensin I converting as possible markers in hypertension program by intrauterine malnutrition

Abstract

The unfavorable nutritional status during the early stages of development, can alter the function of organs and tissues, "metabolically programming" individuals to the onset of maturity. The intrauterine malnutrition is a medical condition that has been associated with kidney disease, type 2 diabetes and hypertension as a consequence of fetal programming. The kidney plays a key role in the development of hypertension programmed by intrauterine malnutrition, with the participation of the renin angiotensin system (RAS) in the etiology of this disease. The RAS plays an important role in blood pressure regulation where the angiotensin I converting enzyme (ACE) cleaves angiotensin I to angiotensin II, a vasoconstrictor petídeo. Studies from our group, detected in the urine of normal individuals, ACE isoforms of 190 and 65 kDa, and urine of hypertensive patients isoforms of 90 and 65 kDa, the 90 kDa isoform is described as a genetic marker hypertension. The objective of this study will be investigate the profile of ACE isoforms, in particular isoforms N-domain of ACE, 90 and 65 kDa, this study model, as well as levels of angiotensins. For this, a couple of rats, and will be mated when detected probable conception, females will be separated into two groups: Control (C), fed ad libitum, and Malnourished group (D), underwent food restriction. After the birth of the offspring will be maintained groups C and D, respectively. At 4 months of age, the animals will be sacrificed, collected serum, plasma and tissues for assay of ACE activity, levels of angiotensins and analysis of protein expression of ACE. We expect to find a correlation between the expression of RAS components, with the physiological manifestations relevant to hypertension preprogrammed. (AU)

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