Rademaker M T, Charles C J, Espiner E A, Frampton C M, Nicholls M G, Richards A M
Department of Medicine, Christchurch School of Medicine, New Zealand.
Am J Physiol. 1996 Feb;270(2 Pt 2):H594-602. doi: 10.1152/ajpheart.1996.270.2.H594.
The responses of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were investigated in six conscious sheep paced at 120, 155, 190, and 225 beats/min for 1.5 h at each rate and at 180, 225, and 180 beats/min for 4 days at each rate. Increased pacing reduced arterial pressure, cardiac output, and urine and Na excretion and increased left atrial pressure and plasma ANP, BNP, and C-type natriuretic peptide, with delayed activation of the renin-angiotensin system (RAS). Acute pacing increased plasma ANP and BNP levels 8.6- and 3.6-fold, respectively (both P < 0.001), whereas chronic pacing increased ANP and BNP 7.8- and 9-fold, respectively (both P < 0.001). Thus the ANP-to-BNP ratio increased during acute pacing (P < 0.001) and decreased proportionately during chronic pacing (P < 0.05). Reduction in pacing improved hemodynamic status, reduced natriuretic peptides (BNP less than ANP), normalized the RAS, and induced diuresis and natriuresis. In conclusion, BNP is less responsive than ANP to acute changes in intracardiac pressure but is proportionately more responsive to chronic hemodynamic changes such as occur in congestive heart failure.
研究了六只清醒绵羊在心率分别为120、155、190和225次/分钟时，以每种心率起搏1.5小时，以及在心率分别为180、225和180次/分钟时，以每种心率起搏4天的情况下，心房利钠肽（ANP）和脑利钠肽（BNP）的反应。起搏频率增加会降低动脉压、心输出量、尿液和钠排泄，并增加左心房压力以及血浆ANP、BNP和C型利钠肽，同时肾素-血管紧张素系统（RAS）的激活延迟。急性起搏使血浆ANP和BNP水平分别升高8.6倍和3.6倍（均P<0.001），而慢性起搏使ANP和BNP分别升高7.8倍和9倍（均P<0.001）。因此，急性起搏期间ANP与BNP的比值升高（P<0.001），而慢性起搏期间该比值成比例降低（P<0.05）。起搏频率降低可改善血流动力学状态，降低利钠肽（BNP降低幅度小于ANP），使RAS恢复正常，并诱导利尿和利钠作用。总之，BNP对心内压急性变化的反应不如ANP敏感，但对慢性血流动力学变化（如在充血性心力衰竭中出现的变化）的反应则相对更敏感。
