[1] Harwani SC, Chapleau MW, Legge KL, et al. Neurohormonal modulation of the innate immune system is proinflammatory in the prehypertensive spontaneously hypertensive rat, a genetic model of essential hypertension[J]. Circ Res, 2012, 111(9): 1190-1197. [2] Ma SK, Choi JS, Joo SY, et al. Activation of the renal PI3K/Akt/mTOR signaling pathway in a DOCA-salt model of hypertension [J]. Chonnam Med J, 2012, 48(3): 150-154. [3] Campos RR, Oliveira-Sales EB, Nishi EE, et al. The role of oxidative stress in renovascular hypertension[J]. Clin Exp Pharmacol Physiol, 2011, 38(2): 144-152. [4] 汪祥海, 武卫, 杨玉雯, 等. Rho激酶信号通路在两肾一夹肾性高血压大鼠心肌肥大中的作用及Fasudil干预[J]. 中国临床药理学与治疗学, 2008, 13(6): 657-662. [5] Gao S, Long CL, Wang RH, et al. KATP activation prevents progression of cardiac hypertrophy to failure induced by pressure overload via protecting endothelial function[J]. Cardiovasc Res, 2009, 83(3): 444-456. [6] Dao HH, Essalihi R, Graillon JF, et al. Pharmacological prevention and regression of arterial remodeling in a rat model of isolated systolic hypertension[J]. J Hypertens, 2002, 20(8): 1597-1606. [7] Mitchell KD, Botros FT, Navar LG. Intrarenal renin-angiotensin system and counter acting protective mechanisms in angiotensin II-dependent hypertension[J]. Acta Physiol Hung, 2007, 94(1/2): 31-48. [8] Shah DM. Role of the renin-angiotensin system in the pathogenesis of preeclampsia[J]. Am J Physiol Renal Physiol, 2005, 288(4): F614-F625. [9] Frey N, Luedde M, Katus HA. Mechanisms of disease: hypertrophic cardiomyopathy[J]. Nat Rev Cardiol, 2011, 9(2): 91-100. [10]Berenji K, Drazner MH, Rothermel BA, et al. Does load-induced ventricular hypertrophy progress to systolic heart failure[J]? Am J Physiol-Heart Circ Physiol, 2005, 289(1): H8-H16. [11]Guimaraes DA, Rizzi E, Ceron CS, et al. Doxycycline dose-dependently inhibits MMP-2-mediated vascular changes in 2K1C hypertension[J]. Basic Clin Pharmacol Toxicol, 2011, 108(5): 318-325. [12]Wagenseil JE, Knutsen RH, Li DY, et al. Elastin-insufficient mice show normal cardiovascular remodeling in 2K1C hypertension despite higher baseline pressure and unique cardiovascular architecture [J]. Am J Physiol-Heart Circ Physiol, 2007, 293(1): H574-H582. |