Ahlborg G, Lundberg J M
Department of Clinical Physiology, Huddinge University Hospital, Sweden.
J Appl Physiol (1985). 1997 May;82(5):1593-600. doi: 10.1152/jappl.1997.82.5.1593.
Healthy men received NG-monomethyl-L-arginine (L-NMMA) intravenously to study cardiovascular and metabolic effects of nitric oxide synthase blockade and whether this alters the response to endothelin-1 (ET-1) infusion. Controls only received ET-1. L-NMMA effects were that heart rate (17%) cardiac output (17%), and splanchnic and renal blood flow (both 33%) fell promptly (all P < 0.01). Mean arterial blood pressure (6%), and systemic (28%) and pulmonary (40%) vascular resistance increased (P < 0.05 to 0.001). Arterial ET-1 levels (21%) increased due to a pulmonary net ET-1 release (P < 0.05 to 0.01). Splanchnic glucose output (SGO) fell (26%, P < 0.01). Arterial insulin and glucagon were unchanged. Subsequent ET-1 infusion caused no change in mean arterial pressure, heart rate, or cardiac output, as found in the present controls, or in splanchnic and renal blood flow or splanchnic glucose output as previously found with ET-1 (G. Ahlborg, E. Weitzberg, and J. M. Lundberg. J. Appl. Physiol. 79: 141-145, 1995). In conclusion, L-NMMA like ET-1, induces prolonged cardiovascular effects and suppresses SGO. L-NMMA causes pulmonary ET-1 release and blocks responses to ET-1 infusion. The results indicate that nitric oxide inhibits ET-1 production and thereby interacts with ET-1 regarding increase in vascular tone and reduction of SGO in humans.
健康男性静脉注射N - 甲基 - L - 精氨酸（L - NMMA），以研究一氧化氮合酶阻断对心血管和代谢的影响，以及这是否会改变对内皮素 - 1（ET - 1）输注的反应。对照组仅接受ET - 1。L - NMMA的作用是心率（下降17%）、心输出量（下降17%）、内脏和肾血流量（均下降33%）迅速下降（均P < 0.01）。平均动脉血压（上升6%）、全身血管阻力（上升28%）和肺血管阻力（上升40%）增加（P < 0.05至0.001）。由于肺部ET - 1净释放，动脉ET - 1水平（上升21%）升高（P < 0.05至0.01）。内脏葡萄糖输出（SGO）下降（26%，P < 0.01）。动脉胰岛素和胰高血糖素水平未改变。随后输注ET - 1，平均动脉血压、心率或心输出量未发生变化，正如本研究对照组中所观察到的，内脏和肾血流量或内脏葡萄糖输出也未发生变化，如同先前用ET - 1所发现的那样（G. 阿尔伯格、E. 魏茨伯格和J. M. 伦德伯格。《应用生理学杂志》79: 141 - 145, 1995）。总之，L - NMMA与ET - 1一样，会诱导长期的心血管效应并抑制SGO。L - NMMA导致肺部ET - 1释放并阻断对ET - 1输注的反应。结果表明，一氧化氮抑制ET - 1的产生，从而在人类血管张力增加和SGO降低方面与ET - 1相互作用。
