Delacrétaz E, Hayoz D, Osterheld M C, Genton C Y, Brunner H R, Waeber B
Division of Hypertension, University Hospital, Lausanne, Switzerland.
Hypertension. 1994 Jun;23(6 Pt 2):967-70. doi: 10.1161/01.hyp.23.6.967.
The goal of the present study was to evaluate the effect of long-term nitric oxide synthase inhibition by NG-nitro-L-arginine-methyl ester (L-NAME) on the morphology and viscoelastic properties of the carotid arteries in rats. Twelve-week-old Wistar-Kyoto rats were treated for 6 weeks with either the nitric oxide synthase inhibitor L-NAME (0.4 g/L in drinking water; L-NAME rats, n = 13) or tap water (control rats, n = 13). Age-matched spontaneously hypertensive rats (SHR, n = 14) received tap water for the same period. The internal diameter of the common carotid artery was measured continuously with an echo-tracking device with the rats under anesthesia with halothane. Intra-arterial pressure was monitored on the contralateral side. L-NAME rats exhibited arterial pressures similar to those of SHR. The distensibility pressure-curve determined in L-NAME rats was a direct continuation of that obtained in control rats. In contrast the distensibility in SHR was increased (P < .01, SHR versus L-NAME rats). Carotid artery cross-sectional area and left ventricular weight index were increased similarly in SHR and L-NAME rats compared with control rats. Thus the hypertension caused by long-term nitric oxide synthesis inhibition was not associated with the increased arterial distensibility observed in SHR despite similar blood pressure elevations, similar arterial hypertrophy, and consequently similar wall stress. This suggests a role for nitric oxide in regulating the mechanical behavior of arteries exposed to high blood pressure.
本研究的目的是评估通过 NG-硝基-L-精氨酸甲酯(L-NAME)长期抑制一氧化氮合酶对大鼠颈动脉形态和粘弹性的影响。12 周龄的 Wistar-Kyoto 大鼠用一氧化氮合酶抑制剂 L-NAME(饮用水中 0.4 g/L;L-NAME 大鼠,n = 13)或自来水(对照大鼠,n = 13)处理 6 周。年龄匹配的自发性高血压大鼠(SHR,n = 14)在同一时期饮用自来水。在大鼠用氟烷麻醉的情况下,用回声跟踪装置连续测量颈总动脉的内径。对侧监测动脉内压。L-NAME 大鼠的动脉压与 SHR 相似。L-NAME 大鼠中测定的扩张性压力曲线是对照大鼠中获得的曲线的直接延续。相比之下,SHR 中的扩张性增加(P <.01,SHR 与 L-NAME 大鼠相比)。与对照大鼠相比,SHR 和 L-NAME 大鼠的颈动脉横截面积和左心室重量指数同样增加。因此,尽管血压升高相似、动脉肥大相似以及壁应力相似,但长期抑制一氧化氮合成所引起的高血压与 SHR 中观察到的动脉扩张性增加无关。这表明一氧化氮在调节暴露于高血压的动脉的力学行为中起作用。