By Icon Health Publications
It is a 3-in-1 reference e-book. It offers an entire clinical dictionary masking hundreds of thousands of phrases and expressions when it comes to aldosterone. It additionally supplies broad lists of bibliographic citations. eventually, it presents info to clients on tips on how to replace their wisdom utilizing a number of web assets. The booklet is designed for physicians, clinical scholars getting ready for Board examinations, clinical researchers, and sufferers who are looking to get to grips with examine devoted to aldosterone. in case your time is effective, this publication is for you. First, you won't waste time looking out the web whereas lacking loads of proper details. moment, the publication additionally saves you time indexing and defining entries. ultimately, you won't waste money and time printing countless numbers of web content.
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Additional info for Aldosterone - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References
We will use real time RT-PCR and immunofluorescence to determine the role of aldosterone and MAPK pathway on ENaC expression in cultured sensory neurons. We will use 2 assays to assess mechanosensory function in cultured sensory neurons. The importance of ENaC proteins in mechanotransduction will be determined using interference RNA and overexpression of dominant-negative isoforms. The results from this proposal may help define the molecular mechanism of baroreceptor inhibition by aldosterone and provide a better understanding of the mechanism of autonomic dysfunction in hypertension and chronic heart failure.
HTN/ECV excess/nephron hyperfiltration; 2B. intrarenal AnglI excess and/or activation of AnglI-generating elements; and 2C. increased renal vascular reactivity to AnglI. AIM 3 will test the hypothesis that effects of MPR and/or Body-Size Excess are mediated by the AT1 receptor. Subaims will test effects of in vivo AT1R blockade or placebo 3A. on hemodynamic and 3B. on AnglI contractile signaling via classic and EGFR-transactivation routes (using renal vascular reactivity and activated vs total signaling protein abundance in fresh vascular/cortical tissues).
Specific Aim 2 will be to establish that the Dahl S elderly and OVX females maintained on low salt intake will become hypertensive as a result of an activation of the RAS. Estrogen administration will maintain activation of the NO system to suppress the RAS. Blockade of NO formation in low salt animals will increase RAS function, especially in the OVX+estrogen animals. Specific Aim 3 is to determine that high salt fed Dahl S elderly and OVX animals will develop a hypertension that is dependent on the activation of the SNS.