Deng A, Baylis C
Department of Physiology, West Virginia University, Morgantown 26506.
Am J Physiol. 1993 Feb;264(2 Pt 2):F212-5. doi: 10.1152/ajprenal.1993.264.2.F212.
During systemic acute blockade of endogenous endothelial-derived relaxing factor (EDRF) with N-monomethyl-L-arginine (NMA), a significant rise in arterial blood pressure (BP) occurred in the anesthetized rat. Renal vasoconstriction was also seen, with complex changes in glomerular hemodynamics; both preglomerular (RA) and efferent arteriolar (RE) resistances increased, producing a fall in glomerular plasma flow (QA) and a rise in glomerular blood pressure (PGC). The glomerular capillary ultrafiltration coefficient (Kf) was reduced. The net effect was a small fall in single-nephron glomerular filtration rate (SNGFR). To determine the effects of local EDRF blockade, two additional groups were studied with intrarenal administration of NMA; in the first series, one-tenth of the systemic dose was given, which produced no change in BP, a small renal vasoconstriction with an increase in RA, but no change in RE; thus PGC was unaffected. Kf fell, and a small reduction in SNGFR was seen. With a larger intrarenal dose of NMA (one-fifth systemic) a moderate rise in BP occurred, but only RA rose; RE and PGC were unaffected, and Kf and SNGFR fell. These observations suggest that locally produced EDRF controls RA and Kf and that a rise in RE and PGC is only seen with systemic EDRF blockade when a large rise in BP occurs.
在用N-单甲基-L-精氨酸（NMA）对内源性内皮衍生舒张因子（EDRF）进行全身急性阻断期间，麻醉大鼠的动脉血压（BP）显著升高。还观察到肾血管收缩，肾小球血流动力学发生复杂变化；入球小动脉（RA）和出球小动脉（RE）阻力均增加，导致肾小球血浆流量（QA）下降和肾小球血压（PGC）升高。肾小球毛细血管超滤系数（Kf）降低。净效应是单肾单位肾小球滤过率（SNGFR）略有下降。为了确定局部EDRF阻断的影响，另外两组接受肾内注射NMA进行研究；在第一组中，给予全身剂量的十分之一，这对BP没有影响，引起轻微的肾血管收缩，RA增加，但RE没有变化；因此PGC未受影响。Kf下降，SNGFR略有降低。给予更大剂量的肾内NMA（全身剂量的五分之一）时，BP出现适度升高，但仅RA升高；RE和PGC未受影响，Kf和SNGFR下降。这些观察结果表明，局部产生的EDRF控制RA和Kf，并且仅在BP大幅升高的全身EDRF阻断时才会出现RE和PGC升高。
