McAllister A S, Atkinson A B, Johnston G D, Hadden D R, Bell P M, McCance D R
Sir George E. Clark Metabolic Unit, Royal Victoria Hospital, Belfast BT12 6BA, Northern Ireland, U.K.
Clin Sci (Lond). 1999 Aug;97(2):141-7.
There is considerable evidence that endothelium-dependent nitric oxide (NO)-mediated vasodilatation in response to acetylcholine is impaired in essential hypertension, whereas the endothelium-independent response to sodium nitroprusside is normal. More limited data have suggested that there is also reduced vasoconstriction in response to N(G)-monomethyl-L-arginine (L-NMMA), a competitive inhibitor of basal NO release. As it is not known whether endothelial dysfunction in hypertension, if indeed present, is a cause or consequence of the condition, we have studied the normotensive offspring of parents with essential hypertension. Both basal and stimulated vascular responses were examined in 12 normotensive offspring [mean age (+/-S.E.M.) 26.1+/-1.4 years] of parents with essential hypertension and compared with those in 12 age-matched offspring (mean age 25.6+/-1.1 years) of normotensive subjects. Forearm blood flow was measured simultaneously in both arms by venous occlusion plethysmography, both at baseline and during intra-arterial brachial infusion of increasing doses of acetylcholine, sodium nitroprusside, noradrenaline and L-NMMA. There were no significant differences between the groups in the responses to acetylcholine, sodium nitroprusside or noradrenaline. In contrast, the vasoconstrictor response to L-NMMA was significantly blunted in the offspring of hypertensive parents compared with that in the offspring of normotensive parents (P=0.005). Thus endothelial dysfunction, as demonstrated by impaired basal production of NO, is present in subjects at high risk of essential hypertension, and does not occur simply as a consequence of the condition.
有大量证据表明，在原发性高血压患者中，内皮依赖性一氧化氮（NO）介导的对乙酰胆碱的血管舒张反应受损，而对硝普钠的非内皮依赖性反应则正常。更有限的数据表明，对基础NO释放的竞争性抑制剂N（G）-单甲基-L-精氨酸（L-NMMA）的血管收缩反应也降低。由于尚不清楚高血压患者中内皮功能障碍（如果确实存在）是该疾病的原因还是结果，我们研究了原发性高血压患者的血压正常的后代。对12名原发性高血压患者的血压正常的后代[平均年龄（±标准误）26.1±1.4岁]和12名年龄匹配的血压正常受试者的后代（平均年龄25.6±1.1岁）进行了基础和刺激后的血管反应检查。通过静脉阻塞体积描记法同时测量双臂的前臂血流量，测量时间为基线时以及动脉内肱动脉输注递增剂量的乙酰胆碱、硝普钠、去甲肾上腺素和L-NMMA期间。两组在对乙酰胆碱、硝普钠或去甲肾上腺素的反应上没有显著差异。相比之下，与血压正常父母的后代相比，高血压父母的后代对L-NMMA的血管收缩反应明显减弱（P = 0.005）。因此，如基础NO生成受损所证明的内皮功能障碍存在于原发性高血压高危人群中，并非仅仅是该疾病的结果。
