Ingelfinger J R, Jung F, Diamant D, Haveran L, Lee E, Brem A, Tang S S
Pediatric Nephrology Laboratory, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.
Am J Physiol. 1999 Feb;276(2):F218-27. doi: 10.1152/ajprenal.1999.276.2.F218.
The renal proximal tubule (PT) is a major site for a complete tissue renin-angiotensin system (RAS) and produces endogenous angiotensin II (ANG II). The present studies demonstrate autocrine RAS feedback in a line of origin-defective SV40 plasmid transformed immortalized rat PT cells (IRPTC) designated as line 93-p-2-1, which are highly differentiated and express all RAS components. Receptor competition assays and Southern blot following RT-PCR demonstrated that these IRPTC express AT1 and AT2 angiotensin receptor subtypes. Autocrine RAS feedback was examined following exposure to ANG II (10(-8) M), and it was noted that angiotensinogen mRNA increases significantly by 1 h and remains elevated through 24 h. The AT1 blocker losartan prevents this increase. Moreover, ANG II upregulates expression of ANG II receptor mRNA (both AT1 and AT2). Thus the present studies demonstrate positive ANG II feedback with angiotensinogen and ANG II receptors in PTC, suggesting that the main site of such intrarenal feedback in vivo is within PT. ANG II secreted by line 93-p-2-1 is increased by isoproterenol, suggesting beta-adrenergic regulation in IRPTC.
肾近端小管(PT)是完整组织肾素-血管紧张素系统(RAS)的主要部位,并产生内源性血管紧张素II(ANG II)。目前的研究表明,在一株起源缺陷的SV40质粒转化的永生化大鼠PT细胞(IRPTC)系(命名为93-p-2-1)中存在自分泌RAS反馈,这些细胞高度分化并表达所有RAS成分。RT-PCR后的受体竞争分析和Southern印迹表明,这些IRPTC表达AT1和AT2血管紧张素受体亚型。在暴露于ANG II(10^(-8) M)后检测自分泌RAS反馈,发现血管紧张素原mRNA在1小时时显著增加,并在24小时内保持升高。AT1阻滞剂氯沙坦可阻止这种增加。此外,ANG II上调ANG II受体mRNA(AT1和AT2)的表达。因此,目前的研究表明PTC中ANG II与血管紧张素原和ANG II受体存在正反馈,提示体内这种肾内反馈的主要部位在PT内。异丙肾上腺素可增加93-p-2-1分泌的ANG II,提示IRPTC中存在β-肾上腺素能调节。