| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| T Hannken, R Schroeder, R A Stahl, G Wol. Angiotensin II-mediated expression of p27Kip1 and induction of cellular hypertrophy in renal tubular cells depend on the generation of oxygen radicals. Kidney international. vol 54. issue 6. 1999-02-11. PMID:9853257. |
angiotensin ii (ang ii) induces hypertrophy of cultured proximal tubular cells. |
1999-02-11 |
2023-08-12 |
mouse |
| T Hannken, R Schroeder, R A Stahl, G Wol. Angiotensin II-mediated expression of p27Kip1 and induction of cellular hypertrophy in renal tubular cells depend on the generation of oxygen radicals. Kidney international. vol 54. issue 6. 1999-02-11. PMID:9853257. |
we have previously demonstrated that this ang ii-mediated hypertrophy occurs in the g1-phase of the cell cycle and depends on the induction of p27kip1, an inhibitor of g1-phase cyclin/cyclin-dependent kinase complexes. |
1999-02-11 |
2023-08-12 |
mouse |
| J Bartunek, E O Weinberg, M Tajima, S Rohrbach, B H Lorel. Angiotensin II type 2 receptor blockade amplifies the early signals of cardiac growth response to angiotensin II in hypertrophied hearts. Circulation. vol 99. issue 1. 1999-02-10. PMID:9884374. |
we have previously shown that the acute molecular growth response of new protein synthesis and protein kinase c activation in response to angiotensin ii (ang ii) is altered in left ventricular (lv) hypertrophy compared with normal hearts. |
1999-02-10 |
2023-08-12 |
Not clear |
| M O Gray, C S Long, J E Kalinyak, H T Li, J S Karline. Angiotensin II stimulates cardiac myocyte hypertrophy via paracrine release of TGF-beta 1 and endothelin-1 from fibroblasts. Cardiovascular research. vol 40. issue 2. 1999-02-10. PMID:9893729. |
we sought to determine whether angiotensin ii (ang ii) promotes hypertrophy of cardiac directly or via paracrine mechanisms mediated by cardiac fibroblasts. |
1999-02-10 |
2023-08-12 |
Not clear |
| G Wol. Angiotensin II is involved in the progression of renal disease: importance of non-hemodynamic mechanisms. Nephrologie. vol 19. issue 7. 1999-01-07. PMID:9857383. |
our group was the first to demonstrate that ang ii stimulates hypertrophy of cultured proximal tubular cells. |
1999-01-07 |
2023-08-12 |
Not clear |
| G Wol. Angiotensin II is involved in the progression of renal disease: importance of non-hemodynamic mechanisms. Nephrologie. vol 19. issue 7. 1999-01-07. PMID:9857383. |
a neutralizing anti-tgf-beta antibody attenuates the ang ii-induced increase in protein synthesis in mct cells suggesting that the hypertrophy is mediated by synthesis and activation of endogenous tgf-beta. |
1999-01-07 |
2023-08-12 |
Not clear |
| G Wol. Angiotensin II is involved in the progression of renal disease: importance of non-hemodynamic mechanisms. Nephrologie. vol 19. issue 7. 1999-01-07. PMID:9857383. |
proximal tubular cells undergoing ang ii-mediated hypertrophy are arrested in the g1-phase of the cell cycle and express typical g1-phase-associated genes. |
1999-01-07 |
2023-08-12 |
Not clear |
| E I Kalenikova, E A Gorodetskaya, N V Zacharova, A B Shechter, O S Medvede. Perindopril effects on angiotensin I elimination in lung after experimental myocardial injury induced by intracoronary microembolization in rats. Journal of cardiovascular pharmacology. vol 32. issue 4. 1998-12-22. PMID:9781929. |
the embolization per se resulted in focal fibrosis, appearance of hypertrophic and dystrophic cardiac myocytes, and was accompanied by increased ang i clearance (1,479 vs. 314 ml/min in sham group), 1.8-fold decreased [125i]-ang ii arterial level, and decreased r (0.5 vs. 1.2 in sham group; p < 0.05). |
1998-12-22 |
2023-08-12 |
rat |
| R L Skolnick, S E Litwin, W H Barry, K W Spitze. Effect of ANG II on pHi, [Ca2+]i, and contraction in rabbit ventricular myocytes from infarcted hearts. The American journal of physiology. vol 275. issue 5. 1998-12-10. PMID:9815087. |
our findings demonstrate that 1) myocytes after myocardial infarction (post-mi) were significantly larger than normal, 2) post-mi hypertrophy was not accompanied by changes in non-co2 intracellular buffering power, 3) post-mi hypertrophy did not significantly affect the ability of na+/h+ exchange to mediate phi recovery from intracellular acidosis, 4) the stimulatory effect of ang ii (100 nm) on na+/h+ exchange was significantly reduced in post-mi myocytes, 5) in hco-3-buffered solutions, ang ii did not significantly stimulate phi recovery from acidosis in post-mi myocytes, 6) the angiotensin at1 receptor mediates the stimulatory action of ang ii on na+/h+ exchange in normal and post-mi myocytes, and 7) the stimulatory effect of ang ii on the ca2+ transient and contraction was blunted in post-mi myocytes bathed in hepes-buffered solution. |
1998-12-10 |
2023-08-12 |
rabbit |
| H Okunish. [Angiotensin II formation by chymase in the cardiovascular tissue]. Nihon yakurigaku zasshi. Folia pharmacologica Japonica. vol 112. issue 3. 1998-12-08. PMID:9793075. |
accumulating evidence indicating that ang ii is not merely a vasopressor agent but also a growth-promoting factor, which leads to tissue hypertrophy and fibrosis, together with the results our studies lead us to propose the tissue-remodeling roles of chymase-formed ang ii in various cardiovascular diseases: dog neointimal proliferation after angioplasty, hamster cardiomyopathy, etc., in which chymase mrna is increased concordantly with tissue remodeling. |
1998-12-08 |
2023-08-12 |
mouse |
| T O Morgan, J F Aubert, Q Wan. Sodium, angiotensin II, blood pressure, and cardiac hypertrophy. Kidney international. Supplement. vol 67. 1998-11-23. PMID:9736294. |
a low-sodium diet had no significant effect on bp or on cardiac size, but prevented the cardiac hypertrophy produced by ang ii without altering the bp response. |
1998-11-23 |
2023-08-12 |
rat |
| E A Jaimes, J M Galceran, L Rai. Angiotensin II induces superoxide anion production by mesangial cells. Kidney international. vol 54. issue 3. 1998-11-17. PMID:9734602. |
indeed, growth stimulating signals driven by ang ii promote mesangial cell (mc) hypertrophy and extracellular matrix production, prominent features of progressive glomerular injury. |
1998-11-17 |
2023-08-12 |
Not clear |
| G Simon, G Illyes, B Csik. Structural vascular changes in hypertension: role of angiotensin II, dietary sodium supplementation, blood pressure, and time. Hypertension (Dallas, Tex. : 1979). vol 32. issue 4. 1998-11-05. PMID:9774359. |
min-1 ang ii for 12 weeks were examined to distinguish hypertrophy from hyperplasia of vascular muscle. |
1998-11-05 |
2023-08-12 |
rat |
| G Simon, G Illyes, B Csik. Structural vascular changes in hypertension: role of angiotensin II, dietary sodium supplementation, blood pressure, and time. Hypertension (Dallas, Tex. : 1979). vol 32. issue 4. 1998-11-05. PMID:9774359. |
min-1 ang ii for 12 weeks, arterial smooth muscle cell thickness was increased without a change in the number of cell layers (hypertrophy). |
1998-11-05 |
2023-08-12 |
rat |
| M Yano, S Kim, Y Izumi, S Yamanaka, H Iwa. Differential activation of cardiac c-jun amino-terminal kinase and extracellular signal-regulated kinase in angiotensin II-mediated hypertension. Circulation research. vol 83. issue 7. 1998-10-20. PMID:9758646. |
cardiac hypertrophy, induced by chronic ang ii infusion, was preceded by jnk activation without erk activation. |
1998-10-20 |
2023-08-12 |
rat |
| M Yano, S Kim, Y Izumi, S Yamanaka, H Iwa. Differential activation of cardiac c-jun amino-terminal kinase and extracellular signal-regulated kinase in angiotensin II-mediated hypertension. Circulation research. vol 83. issue 7. 1998-10-20. PMID:9758646. |
these results provided the first evidence for the preferential activation of cardiac jnk in ang ii-induced hypertension and suggested that jnk might play some role in ang ii-induced cardiac hypertrophic response in vivo. |
1998-10-20 |
2023-08-12 |
rat |
| S B Parker, S S Wade, R L Prewit. Pressure mediates angiotensin II-induced arterial hypertrophy and PDGF-A expression. Hypertension (Dallas, Tex. : 1979). vol 32. issue 3. 1998-10-15. PMID:9740610. |
angiotensin ii (ang ii) may induce arterial hypertrophy either directly or through an increase in arterial pressure. |
1998-10-15 |
2023-08-12 |
rat |
| S B Parker, S S Wade, R L Prewit. Pressure mediates angiotensin II-induced arterial hypertrophy and PDGF-A expression. Hypertension (Dallas, Tex. : 1979). vol 32. issue 3. 1998-10-15. PMID:9740610. |
these results show that (1) arterial hypertrophy from ang ii infusion occurs in response to elevated arterial pressure, (2) hypertrophy was not associated with hyperplasia or polyploidy of vascular smooth muscle cells, and (3) pdgf-a expression correlated with elevated pressure and arterial wall hypertrophy. |
1998-10-15 |
2023-08-12 |
rat |
| K Kamide, M T Hori, J H Zhu, J D Barrett, P Eggena, M L Tuc. Insulin-mediated growth in aortic smooth muscle and the vascular renin-angiotensin system. Hypertension (Dallas, Tex. : 1979). vol 32. issue 3. 1998-10-15. PMID:9740614. |
because angiotensin i (ang i)-converting enzyme inhibitors have been shown to improve insulin action and to impede the progression of vascular hypertrophy in hypertensive animal models, it is possible that the vascular properties of insulin may be mediated through the tissue renin-angiotensin system (ras). |
1998-10-15 |
2023-08-12 |
rat |
| A M Zafari, M Ushio-Fukai, M Akers, Q Yin, A Shah, D G Harrison, W R Taylor, K K Griendlin. Role of NADH/NADPH oxidase-derived H2O2 in angiotensin II-induced vascular hypertrophy. Hypertension (Dallas, Tex. : 1979). vol 32. issue 3. 1998-10-15. PMID:9740615. |
we previously showed that angiotensin ii (ang ii) increases superoxide production by activating an nadh/nadph oxidase, which contributes to hypertrophy. |
1998-10-15 |
2023-08-12 |
Not clear |