Leskinen H, Ruskoaho H, Huttunen P, Leppäluoto J, Vuolteenaho O
Department of Physiology, University of Oulu, Finland.
Am J Physiol. 1994 Jun;266(6 Pt 2):R1933-43. doi: 10.1152/ajpregu.1994.266.6.R1933.
We examined the effect of hemorrhage on plasma NH2-terminal pro-atrial natriuretic peptide (NT-pro-ANP) and atrial natriuretic peptide (ANP) in anesthetized and conscious rats. Blood (1.5 ml/time point) was withdrawn at 0, 10, 20, and 30 min. In anesthetized rats it caused decrease in mean arterial pressure and led to bradycardia in 2 min. Right atrial pressure decreased significantly after 12 min. However, plasma ANP did not change, and NT-pro-ANP actually increased from 481 +/- 55 to 609 +/- 73 pmol/l (P < 0.01) at 20 min and to 696 +/- 82 pmol/l (P < 0.01) at 30 min. Also plasma arginine-8-vasopressin (AVP) and epinephrine increased significantly at 30 min. No significant changes in plasma endothelin and norepinephrine were found. The increase in NT-pro-ANP after hemorrhage was not blocked by AVP V1-receptor, alpha- and beta-catecholaminergic receptor, or muscarinic-receptor antagonists. The plasma 125I-ANP disappearance curve was shifted to the right after hemorrhage in anesthetized rats, suggesting that the elimination of ANP was decreased. In conscious rats, heart rate and right atrial pressure did not change significantly after hemorrhage, and mean arterial pressure did not decrease until 22 min. NT-pro-ANP decreased from 1,467 +/- 146 to 1,072 +/- 130 pmol/l (P < 0.01) at 20 min and to 941 +/- 41 pmol/l (P < 0.01) at 30 min. Plasma ANP did not respond to hemorrhage in conscious rats. In conclusion, we found no change in plasma ANP during hemorrhage in either anesthetized or conscious rats, but we did find a significant increase in plasma NT-pro-ANP levels in anesthetized rats and a significant decrease in conscious rats. We suggest that this divergence may be due to different hemodynamic responses to hemorrhage.
我们研究了出血对麻醉和清醒大鼠血浆氨基末端前心钠素（NT-pro-ANP）和心钠素（ANP）的影响。在0、10、20和30分钟时采血（1.5毫升/时间点）。在麻醉大鼠中，出血导致平均动脉压下降，并在2分钟内引起心动过缓。12分钟后右心房压力显著下降。然而，血浆ANP没有变化，NT-pro-ANP在20分钟时实际上从481±55升高到609±73皮摩尔/升（P<0.01），在30分钟时升高到696±82皮摩尔/升（P<0.01）。此外，血浆精氨酸-8-血管加压素（AVP）和肾上腺素在30分钟时显著升高。血浆内皮素和去甲肾上腺素未发现显著变化。出血后NT-pro-ANP的升高未被AVP V1受体、α和β肾上腺素能受体或毒蕈碱受体拮抗剂阻断。麻醉大鼠出血后血浆125I-ANP消失曲线右移，提示ANP的清除减少。在清醒大鼠中，出血后心率和右心房压力无显著变化，平均动脉压直到22分钟才下降。NT-pro-ANP在20分钟时从1467±146下降到1072±130皮摩尔/升（P<0.01），在30分钟时下降到941±41皮摩尔/升（P<0.01）。清醒大鼠血浆ANP对出血无反应。总之，我们发现在麻醉或清醒大鼠出血期间血浆ANP没有变化，但我们确实发现麻醉大鼠血浆NT-pro-ANP水平显著升高，清醒大鼠则显著降低。我们认为这种差异可能是由于对出血的血流动力学反应不同所致。
