Renin angiotensin system induced secondary hypertension: The alteration of kidney function and structure

Zahra Pezeshki ©, Mehdi Nematbakhsh

Renin angiotensin system induced secondary hypertension: The alteration of kidney function and structure

کد: G-03251

نویسندگان: Zahra Pezeshki ©, Mehdi Nematbakhsh

زمان بندی: زمان بندی نشده!

برچسب: فیزیولوژی و فارماکولوژی

دانلود: دانلود پوستر

خلاصه مقاله:

Background and Aim

Long-term hypertension is known as a major risk factor for cardiovascular and chronic kidney disease (CKD). Renin angiotensin system (RAS) plays a key role in hypertension pathogenesis. Angiotensin II (Ang II) enhancement in Ang II dependent hypertension lead to progressive CKD.


Based on a variety of sources including PubMed, Google Scholar, Scopus and Science-Direct, in current review we will discuss the role of RAS induced secondary hypertension on the alteration of renal function.


In two kidney one clip model (2K1C) more renin is synthesized in the principal cells of collecting duct than juxtaglomerular cells (JGC). An increase of renal Ang I and Ang II levels, and a decrease of renal cortical and medullary of Ang 1-7 occur in both kidneys of 2K1C hypertensive rat model. Also change the balance in production of renal ACE, ACE2 and PrCP expression. Intra-renal angiotensiogen (AGT) expression and urine AGT (uAGT) excretion rates in unclipped kidney are greater than clipped kidney in 2K1C hypertensive rat model. The enhancement of Ang II in clipped kidney is related to renin secretion, while the elevation of intrarenal Ang II in unclipped kidney is related to stimulation of AGT mRNA and protein in proximal tubule cells by direct effect of systemic Ang II level. Ang II dependent increases cytokines, which stimulate AGT synthesis in proximal tubules. Accumulation of inflammatory cells in the kidney aggravates hypertension and renal damage. Moreover, Ang II dependent hypertension alters renal Ang II type 1 & 2 receptors (AT1R & AT2R) and Mas receptor (MasR) expression, and the renal interstitial fluid bradykinine, nitric oxide, and cGMP response to AT1R, AT2R, or BK B2-receptor antagonists.


Ang II dependent hypertension affect local renal RAS components and function.


Renin angiotensin system; Hypertension; Renal function

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