Ganger D R, Gottstein J, Blei A T
Department of Medicine, Veterans Administration Lakeside Medical Center, Chicago, Illinois.
J Pharmacol Exp Ther. 1988 Sep;246(3):941-5.
The effects of atrial natriuretic factor (ANF) on splanchnic hemodynamics and renal function in portal hypertensive models are described incompletely. Furthermore, ANF-induced vasodilatation and hypotension may limit the assessment of its own renal physiological effects. We infused ANF (human ANF 102-126) to anesthetized portal vein-ligated rats, a model with prehepatic portal hypertension. Arterial pressure was reduced by 17%, but portal pressure was unaffected. Diuresis and natriuresis were explained in part by an increase in glomerular filtration rate; in addition, renal vascular resistance was significantly decreased. The natriuretic response to ANF was slightly, but significantly, decreased in portal hypertensive rats as compared to controls (fractional excretion of sodium, 1.8 +/- 0.4 vs. 2.9 +/- 0.3; P less than .05). The addition of Phe-Ile-Orn-vasopressin, a V1 receptor agonist, normalized arterial pressure but induced a significant decrease in portal pressure (15 +/- 0.9 mm Hg base line vs. 12.8 +/- 0.7 combination group; P less than .01). Furthermore, the combination of both drugs markedly potentiated the natriuretic effects (0.4 +/- 0.1 microEq/min of control vs. 10.0 +/- 2.3 ANF vs. 32.2 +/- 3.3 combination group; P less than .001). The natriuretic potentiation resulted from increments in glomerular filtration rate and renal blood flow. Normalization of arterial pressure may enhance the renal physiological effects of ANF, in this portal hypertensive model.
心房利钠因子（ANF）对门脉高压模型内脏血流动力学及肾功能的影响尚未完全阐明。此外，ANF诱导的血管舒张和低血压可能会限制对其自身肾脏生理效应的评估。我们将ANF（人ANF 102 - 126）注入麻醉的门静脉结扎大鼠（一种肝前门脉高压模型）体内。动脉压降低了17%，但门静脉压未受影响。利尿和利钠作用部分是由于肾小球滤过率增加所致；此外，肾血管阻力显著降低。与对照组相比，门脉高压大鼠对ANF的利钠反应略有但显著降低（钠排泄分数，1.8±0.4对2.9±0.3；P＜0.05）。添加V1受体激动剂苯丙氨酸 - 异亮氨酸 - 鸟氨酸 - 血管加压素可使动脉压恢复正常，但会导致门静脉压显著降低（基线时为15±0.9 mmHg，联合用药组为12.8±0.7 mmHg；P＜0.01）。此外，两种药物联合使用显著增强了利钠作用（对照组为0.4±0.1微当量/分钟，ANF组为10.0±2.3，联合用药组为32.2±3.3；P＜0.001）。利钠作用增强是由于肾小球滤过率和肾血流量增加所致。在这个门脉高压模型中，动脉压恢复正常可能会增强ANF的肾脏生理效应。
