Brady Felicity, Bakhle Y S, Bell C
Department of Physiology, Trinity College, Dublin, Ireland.
Acta Physiol Hung. 2002;89(4):451-61. doi: 10.1556/APhysiol.89.2002.4.5.
The attenuation of baroreflex gain associated with hereditary hypertension could involve abnormal signalling by nitric oxide or substance P. Baroreflex gain was measured in age-matched male genetically hypertensive (GH) and nonnotensive (N) anaesthetised rats from heart rate changes in response to i.v. phenylephrine or sodium nitroprusside. In subgroups of these animals, nitric oxide synthesis was inhibited using NG-nitro-L-arginine methyl ester (L-NAME, 30 mg x kg(-1) i.v.), substance P transmission was blocked using the antagonist SR 140333 (360 nmoles x kg(-1) i.v.) or substance P release was inhibited with resiniferatoxin (4 doses of 0.3 microg x kg(-1) i.v. at 4 min intervals). Baroreflex gain was markedly reduced in GH compared to N animals (N -0.37 +/- 0.04 beat x min(-1) x mm Hg(-1), GH -0.17 +/- 0.02 beat x min(-1) x mm Hg(-1), p < 0.0001). Inhibition of nitric oxide synthase increased baroreflex gain in each strain, but the inter-strain difference in gain persisted (post-treatment N -0.57 +/- 0.07 beat x min(-1) x mm Hg(-1), GH -0.24 +/- 0.05 beat x min(-1) x mm Hg(-1) (p < 0.001). Blockade of receptors or inhibition of substance P release did not affect gain in either strain. Nitric oxide, but not substance P, appears to play an inhibitory role in the rat arterial baroreflex. Impairment of baroreflex gain in GH rats is not secondary to altered nitric oxide signaling.
与遗传性高血压相关的压力反射增益减弱可能涉及一氧化氮或P物质的信号异常。通过静脉注射去氧肾上腺素或硝普钠后心率的变化，测量年龄匹配的雄性遗传性高血压（GH）和血压正常（N）麻醉大鼠的压力反射增益。在这些动物的亚组中，使用NG-硝基-L-精氨酸甲酯（L-NAME，30mg·kg⁻¹静脉注射）抑制一氧化氮合成，使用拮抗剂SR 140333（360nmol·kg⁻¹静脉注射）阻断P物质传递，或用树脂毒素（4剂，0.3μg·kg⁻¹静脉注射，间隔4分钟）抑制P物质释放。与N组动物相比，GH组的压力反射增益明显降低（N组为-0.37±0.04次·分钟⁻¹·mmHg⁻¹，GH组为-0.17±0.02次·分钟⁻¹·mmHg⁻¹，p<0.0001）。抑制一氧化氮合酶可增加每个品系的压力反射增益，但品系间的增益差异仍然存在（处理后N组为-0.57±0.07次·分钟⁻¹·mmHg⁻¹，GH组为-
