Macedo M P, Lautt W W
Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Am J Physiol. 1997 Mar;272(3 Pt 1):G507-14. doi: 10.1152/ajpgi.1997.272.3.G507.
Our objective was to determine the vasodilator effect of adenosine and isoproterenol on the hepatic artery (HA) and superior mesenteric artery (SMA) before and after blockade of nitric oxide (NO) production to evaluate the possibility of organ specificity. Vascular circuits supplied blood flow to the liver or intestine in cats under pentobarbital sodium anesthesia. The NO synthase (NOS) antagonist N(G)-nitro-L-arginine methyl ester (L-NAME; 2.5 mg/kg iv) increased arterial pressure from 106.4 +/- 7.6 to 141.4 +/- 8.1 mmHg and raised basal vascular tone in the SMA but not in the HA. The NOS substrate L-arginine (75 mg/kg) reversed these effects. The decrease in perfusion pressure in response to adenosine was 51.7 +/- 2.9, 135.2 +/- 6.1, and 16.7 +/- 2.4 mmHg, respectively, for control and after L-NAME and L-arginine. Isoproterenol was also potentiated in the SMA. Adenosine and isoproterenol were not potentiated in the HA by L-NAME. Potentiation did not occur when HA or SMA basal tone was elevated by norepinephrine. In conclusion, L-NAME increased basal tone for the SMA and potentiated the dilation induced by adenosine and isoproterenol in the SMA but not in the HA. This study provides evidence that there is a highly organ-specific compensatory mechanism in which the absence of NO promotes potentiation of other vasodilators.
我们的目的是在一氧化氮（NO）生成被阻断前后，测定腺苷和异丙肾上腺素对肝动脉（HA）和肠系膜上动脉（SMA）的血管舒张作用，以评估器官特异性的可能性。在戊巴比妥钠麻醉下，血管回路为猫的肝脏或肠道供应血流。一氧化氮合酶（NOS）拮抗剂N(G)-硝基-L-精氨酸甲酯（L-NAME；2.5mg/kg静脉注射）使动脉压从106.4±7.6mmHg升高至141.4±8.1mmHg，并提高了SMA的基础血管张力，但对HA没有影响。NOS底物L-精氨酸（75mg/kg）可逆转这些作用。在对照、L-NAME处理后和L-精氨酸处理后，腺苷引起的灌注压下降分别为51.7±2.9、135.2±6.1和16.7±2.4mmHg。异丙肾上腺素在SMA中也有增强作用。L-NAME对HA中的腺苷和异丙肾上腺素没有增强作用。当HA或SMA的基础张力由去甲肾上腺素升高时，增强作用未发生。总之，L-NAME增加了SMA的基础张力，并增强了腺苷和异丙肾上腺素在SMA中诱导的舒张作用，但在HA中没有。本研究提供了证据，表明存在一种高度器官特异性的代偿机制，其中NO的缺乏促进了其他血管舒张剂的增强作用。
