Alvarez Violeta, Quiroz Yasmir, Nava Mayerly, Pons Héctor, Rodríguez-Iturbe Bernardo
Renal Service and Laboratory and Instituto de Investigaciones Biomédicas, Fundacite-Zulia, Hospital Universitario, Universidad del Zulia, Maracaibo 4001-A, Venezuela.
Am J Physiol Renal Physiol. 2002 Nov;283(5):F1132-41. doi: 10.1152/ajprenal.00199.2002.
Recent evidence suggests that salt-sensitive hypertension develops as a consequence of renal infiltration with immunocompetent cells. We investigated whether proteinuria, which is known to induce interstitial nephritis, causes salt-sensitive hypertension. Female Lewis rats received 2 g of BSA intraperitoneally daily for 2 wk. After protein overload (PO), 6 wk of a high-salt diet induced hypertension [systolic blood pressure (SBP) = 156 +/- 11.8 mmHg], whereas rats that remained on a normal-salt diet and control rats (without PO) on a high-salt diet were normotensive. Administration of mycophenolate mofetil (20 mg. kg(-1). day(-1)) during PO resulted in prevention of proteinuria-related interstitial nephritis, reduction of renal angiotensin II-positive cells and oxidative stress (superoxide-positive cells and renal malondialdehyde content), and resistance to the hypertensive effect of the high-salt diet (SBP = 129 +/- 12.2 mmHg). The present studies support the participation of renal inflammatory infiltrate in the pathogenesis of salt-sensitive hypertension and provide a direct link between two risk factors of progressive renal damage: proteinuria and hypertension.
近期证据表明，盐敏感性高血压是免疫活性细胞浸润肾脏的结果。我们研究了已知可诱发间质性肾炎的蛋白尿是否会导致盐敏感性高血压。雌性Lewis大鼠每天腹腔注射2 g牛血清白蛋白，持续2周。蛋白超负荷（PO）后，6周的高盐饮食诱发了高血压[收缩压（SBP）= 156±11.8 mmHg]，而维持正常盐饮食的大鼠以及高盐饮食的对照大鼠（无PO）血压正常。在PO期间给予霉酚酸酯（20 mg·kg-1·天-1）可预防蛋白尿相关的间质性肾炎，减少肾血管紧张素II阳性细胞和氧化应激（超氧化物阳性细胞和肾丙二醛含量），并抵抗高盐饮食的高血压作用（SBP = 129±12.2 mmHg）。本研究支持肾脏炎性浸润参与盐敏感性高血压的发病机制，并在进行性肾损伤的两个危险因素：蛋白尿和高血压之间建立了直接联系。
