一氧化氮对犬膈肌基线血管阻力的调节作用。

Regulation of baseline vascular resistance in the canine diaphragm by nitric oxide.

Ward M E, Hussain S N

Division of Pulmonary and Critical Care Medicine, Royal Victoria Hospital, Montreal, Quebec, Canada.

Br J Pharmacol. 1994 May;112(1):65-70. doi: 10.1111/j.1476-5381.1994.tb13030.x.

Abstract

The role played by nitric oxide (NO) in the regulation of blood flow to the canine isolated hemidiaphragm was evaluated by determining (a) the effects of the L-arginine analogues NG-nitro-L-arginine methyl ester (L-NAME), NG-nitro-L-arginine (L-NOARG), and argininosuccinic acid (ArgSA) on baseline vascular resistance and of the latter two agents on endothelium-dependent (acetylcholine, ACh) and endothelium independent (sodium nitroprusside, SNP) vasodilatation; (b) the effects of L- and D-arginine on baseline vascular resistance; and (c) the effects of L-glutamine, an inhibitor of intracellular recycling of L-citrulline to L-arginine, on baseline resistance and on the response to ACh and SNP. 2. L-NAME, L-NOARG and ArgSA (6 x 10(-4) M final concentration) increased baseline diaphragmatic vascular resistance to a similar extent (28.6 +/- 4.2%, 26.7 +/- 4.3% and 32.8 +/- 4.6% respectively). L-NOARG and ArgSA reversed the vasodilator effect of ACh but not of SNP. 3. L- and D-arginine had no effect on vascular resistance. 4. L-Glutamine (10(-3) M) increased baseline vascular resistance by 10 +/- 1.9% (P < 0.05) but did not alter responses to either ACh or SNP. 5. Basal NO release plays a role in the regulation of baseline diaphragmatic vascular resistance. L-Arginine analogues tested potently and specifically inhibited this process. Moreover, extracellular L-arginine appears to have no effect on baseline diaphragmatic vascular resistance.

摘要

通过测定以下各项来评估一氧化氮（NO）在调节犬离体半膈血流量中的作用：（a）L-精氨酸类似物N G-硝基-L-精氨酸甲酯（L-NAME）、N G-硝基-L-精氨酸（L-NOARG）和精氨琥珀酸（ArgSA）对基础血管阻力的影响，以及后两种药物对内皮依赖性（乙酰胆碱，ACh）和非内皮依赖性（硝普钠，SNP）血管舒张的影响；（b）L-精氨酸和D-精氨酸对基础血管阻力的影响；（c）L-谷氨酰胺（一种将L-瓜氨酸再循环为L-精氨酸的细胞内抑制剂）对基础阻力以及对ACh和SNP反应的影响。2. L-NAME、L-NOARG和ArgSA（终浓度6×10⁻⁴M）使基础膈血管阻力增加到相似程度（分别为28.6±4.2%、26.7±4.3%和32.8±4.6%）。L-NOARG和ArgSA可逆转ACh的血管舒张作用，但不能逆转SNP的血管舒张作用。3. L-精氨酸和D-精氨酸对血管阻力无影响。4. L-谷氨酰胺（10⁻³M）使基础血管阻力增加10±1.9%（P<0.05），但不改变对ACh或SNP的反应。5. 基础NO释放参与基础膈血管阻力的调节。所测试的L-精氨酸类似物有效且特异性地抑制了这一过程。此外，细胞外L-精氨酸似乎对基础膈血管阻力无影响。