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Additional info for Aldosterone - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References
The first specific hypothesis is that the aging process with the accompanying loss of estrogen activity is associated with a down regulation of the nitric oxide system resulting in hypertension. To test this hypothesis, Specific Aim 1 of this study is to monitor blood pressure and the level of activation of the NO system in intact, ovariectomized (OVX), and OVX+estrogen-treated Dahl salt sensitive and Dahl salt-resistant (R) female rats as they age from 3 month to 2022 months of age. The second specific hypothesis is that the factors maintaining the hypertension associated with the loss of estrogen activity in Dahl S rats is determined by the level of salt intake.
In addition, salt sensitivity is more prevalent among African Americans and has been postulated to contribute to both hypertension and hypertensive nephropathy. Animal models provide excellent opportunities for examining specific regulatory systems that can then be translated into clinical trials. Studies by the investigator's previous group have shown that Gamma Melanocyte Stimulating Hormone (gammaMSH), a potent natriuretic peptide, plays a role in normal sodium homeostasis in rats. They demonstrated that Sprague Dawley (SD) rats have increased pituitary prohormone proopiomelanocortin (POMC) and protease convertases (PC1 and PC2 that process the POMC into [gammaMSH) mRNA expressions along with an increase in plasma gammaMSH level at 3 weeks of chronic salt loading, suggesting a possible role of this system (gammaMSH system) in sodium homeostasis.
A full fibrotic response was restored by infusion of angiotensin or aldosterone, together with restoration of local increase of PAI-1. These projects will examine the TGFbeta1 dependent and independent mechanisms of fibrosis. We hypothesize that PAI-1 induction occurs even in the absence of local TGFbeta, and that PAI-1 by itself can effect fibrosis. We further hypothesize that both parenchymal and infiltrating cell mechanisms are necessary for full fibrotic response. We postulate that injury promotes epithelial-mesenchymal transdifferentiation, and that inadequate macrophage clearance of apoptotic cells both contribute to fibrosis.