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      Mechanical Stretch/Relaxation Stimulates a Cellular Renin-Angiotensin System in Cultured Rat Mesangial Cells

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          Angiotensin II (Ang II) may play a significant role mediating intraglomerular hypertension and glomerular sclerosis. Therefore, we investigated whether a model of pressure-induced stress, mechanical stretch/relaxation, affected the renin-angiotensin system (RAS) in cultured rat mesangial cells. Type 1 Ang II receptor (AT<sub>1</sub>R) expression was assessed by <sup>125</sup>I-Ang II binding and quantitative reverse-transcription polymerase chain reaction. Stretch/relaxation increased steady-state AT<sub>1</sub>R mRNA levels as well as specific [<sup>125</sup>I]Ang II binding. Increased AT<sub>1</sub>R expression was associated with altered AT<sub>1</sub>R signaling. Ang II (100 n M) increased total phosphoinositide hydrolysis in control cells (186 ± 25%, n = 6; p < 0.025 vs. no treatment). However, stretch/relaxation for 48 h further augmented AT<sub>1</sub>R-mediated PI hydrolysis (293 ± 38%, n = 6; p < 0.025 vs. Ang II treatment alone). We examined other RAS components in mesangial cells subjected to stretch/relaxation. Angiotensinogen, determined by radioimmunoassay of Ang I generation in conditioned media, increased with stretch/relaxation, and reverse-transcription polymerase chain reaction demonstrated increased angiotensinogen gene expression in stretch/relaxation-treated cells. However, renin activity and angiotensin-converting-enzyme-like activity were unaffected by stretch/relaxation. Thus, mesangial cells maintain a local RAS similar to those described in other tissues, and AT<sub>1</sub>R expression and angiotensinogen production in this cellular RAS are increased by stretch/relaxation. It is likely that mesangial cells in vivo, exposed to variations in intraglomerular pressure, may regulate their responses via a local RAS.

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          Most cited references 7

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          Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction.

          A new method of total RNA isolation by a single extraction with an acid guanidinium thiocyanate-phenol-chloroform mixture is described. The method provides a pure preparation of undegraded RNA in high yield and can be completed within 4 h. It is particularly useful for processing large numbers of samples and for isolation of RNA from minute quantities of cells or tissue samples.
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            Autocrine release of angiotensin II mediates stretch-induced hypertrophy of cardiac myocytes in vitro.

            Hypertrophy is a fundamental adaptive process employed by postmitotic cardiac and skeletal muscle in response to mechanical load. How muscle cells convert mechanical stimuli into growth signals has been a long-standing question. Using an in vitro model of load (stretch)-induced cardiac hypertrophy, we demonstrate that mechanical stretch causes release of angiotensin II (Ang II) from cardiac myocytes and that Ang II acts as an initial mediator of the stretch-induced hypertrophic response. The results not only provide direct evidence for the autocrine mechanism in load-induced growth of cardiac muscle cells, but also define the pathophysiological role of the local (cardiac) renin-angiotensin system.
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              Stimulation of Transcription Factors NFκB and AP1 in Endothelial Cells Subjected to Shear Stress


                Author and article information

                Nephron Exp Nephrol
                Cardiorenal Medicine
                S. Karger AG
                February 1998
                04 February 1998
                : 6
                : 1
                : 57-66
                Departments of a Medicine and b Pediatrics, Vanderbilt University School of Medicine, and Department of Veterans Affairs Medical Center, Nashville, Tenn., USA c indicates equal contribution by authors
                20505 Exp Nephrol 1998;6:57–66
                © 1998 S. Karger AG, Basel

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                Figures: 8, Tables: 1, References: 49, Pages: 10
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