Peotta V A, Vasquez E C, Meyrelles S S
Physiological Sciences Graduate Program, Biomedical Center, Federal University of Espirito Santo, and Health Sciences College (Emescam), Vitoria, ES, Brazil.
Hypertension. 2001 Sep;38(3 Pt 2):555-9. doi: 10.1161/01.hyp.38.3.555.
The mouse is the most used animal for studying the genetic basis of cardiovascular diseases. However, the mechanisms of regulation of cardiovascular function in this animal are not yet well understood. The goal of this study was to evaluate the baroreflex, the Bezold-Jarisch cardiopulmonary reflex (BJR), and the chemoreflex in mice with hypertension induced by inhibition of NO using Nomega-nitro-L-arginine-methyl ester (L-NAME). Basal mean arterial pressure (MAP) measured under anesthesia (urethane, 1 mg/g IP) was significantly higher in L-NAME (400 microgram/g IP for 7 days)-treated (HT) mice (n=7) compared with vehicle-treated (NT; n=10) animals (126+/-9 versus 79+/-2 mm Hg) without differences in heart rate (HR). Baroreflex sensitivity, evaluated using phenylephrine (1 microgram/g IV) was enhanced in HT mice compared with NT mice (-9.8+/-1.4 versus -4.9+/-0.5 bpm/mm Hg). The BJR, induced by phenylbiguanide (40 ng/g IV), was significantly attenuated in HT animals (MAP, -13+/-5%; HR, -39+/-6%) compared with NT animals (MAP, -38+/-5%; HR, -66+/-2%). The chemoreflex, induced by potassium cyanide (0.26 microgram/g IV), was significantly attenuated in HT animals (MAP, +14+/-4%; HR, -8+/-2%) compared with NT animals (MAP, +29+/-4%; HR, -15+/-4%). As has been observed in rats, chronic inhibition of NO synthase in mice results in arterial hypertension. Enhancement of baroreflex sensitivity and attenuation of BJR and chemoreflex seem to be mainly caused by inhibition of NO synthesis because individual analyses did not show positive correlation between changes in these reflexes and MAP levels in the HT group.
小鼠是研究心血管疾病遗传基础时使用最为广泛的动物。然而，这种动物中心血管功能的调节机制尚未得到充分了解。本研究的目的是评估使用Nω-硝基-L-精氨酸甲酯（L-NAME）抑制一氧化氮（NO）诱导高血压的小鼠的压力反射、贝佐尔德-雅里什心肺反射（BJR）和化学反射。在麻醉（乌拉坦，1mg/g腹腔注射）下测量的基础平均动脉压（MAP），L-NAME（400μg/g腹腔注射，持续7天）处理的（HT）小鼠（n = 7）显著高于溶剂处理的（NT；n = 10）动物（126±9与79±2mmHg），心率（HR）无差异。与NT小鼠相比，HT小鼠使用去氧肾上腺素（1μg/g静脉注射）评估的压力反射敏感性增强（-9.8±1.4与-4.9±0.5bpm/mm Hg）。与NT动物相比，苯乙双胍（40ng/g静脉注射）诱导的BJR在HT动物中显著减弱（MAP，-13±5%；HR，-39±6%）（MAP，-38±5%；HR，-66±2%）。与NT动物相比，氰化钾（0.26μg/g静脉注射）诱导的化学反射在HT动物中显著减弱（MAP，+14±4%；HR，-8±2%）（MAP，+29±4%；HR，-15±4%）。正如在大鼠中所观察到的，小鼠中慢性抑制一氧化氮合酶会导致动脉高血压。压力反射敏感性增强以及BJR和化学反射减弱似乎主要是由一氧化氮合成抑制引起的，因为单独分析未显示HT组中这些反射变化与MAP水平之间存在正相关。
