Blantz R C, Gabbai F B, Tucker B J, Yamamoto T, Wilson C B
Division of Nephrology-Hypertension, University of California San Diego, La Jolla 92093.
Am J Physiol. 1993 Jan;264(1 Pt 2):F158-65. doi: 10.1152/ajprenal.1993.264.1.F158.
We have examined the physiological role of the mesangial cell in the regulation of glomerular hemodynamics utilizing mesangial cell lysis by the administration of antithymocyte antibody serum (ATS) 24 h before micropuncture evaluation. Plasma volume expansion (PVE) in normal NaCl-depleted rats increased single-nephron glomerular filtration rate (SNGFR) by 30% because of increases in single-nephron plasma flow (SNPF), whereas glomerular capillary hydrostatic pressure (PG) remained constant. SNGFR did not increase with PVE in NaCl-depleted ATS rats despite increases in SNPF, and PG increased significantly (51 +/- 2 to 67 +/- 3 mmHg) because of afferent arteriolar dilation, whereas efferent resistance remained elevated. Angiotensin II (ANG II) infusion in normal rats decreased SNGFR because of reductions in SNPF and the glomerular ultrafiltration coefficient (LpA), whereas the hydrostatic pressure gradient (delta P) increased. In ATS rats ANG II infusion did not change SNGFR, LpA, or delta P. These in vivo studies suggest that the mesangial cell plays an important role in the regulation of LpA, efferent arteriolar resistance, and the regulation of PG, whereas this cell exerts little effect on the afferent arteriole.
我们通过在微穿刺评估前24小时给予抗胸腺细胞抗体血清(ATS)来裂解系膜细胞,研究了系膜细胞在肾小球血流动力学调节中的生理作用。正常低钠大鼠的血浆容量扩张(PVE)使单肾单位肾小球滤过率(SNGFR)增加30%,这是由于单肾单位血浆流量(SNPF)增加所致,而肾小球毛细血管静水压(PG)保持恒定。低钠ATS大鼠尽管SNPF增加,但PVE时SNGFR并未增加,且由于入球小动脉扩张,PG显著升高(从51±2 mmHg升高至67±3 mmHg),而出球小动脉阻力仍保持升高。正常大鼠输注血管紧张素II(ANG II)会使SNGFR降低,这是由于SNPF和肾小球超滤系数(LpA)降低,而静水压梯度(ΔP)增加。在ATS大鼠中,输注ANG II并未改变SNGFR、LpA或ΔP。这些体内研究表明,系膜细胞在LpA调节、出球小动脉阻力调节以及PG调节中起重要作用,而该细胞对入球小动脉影响很小。