Cargill R I, Coutie W J, Lipworth B J
Department of Clinical Pharmacology, Ninewells Hospital and Medical School, Dundee, Scotland, UK.
Br J Clin Pharmacol. 1994 Aug;38(2):139-42. doi: 10.1111/j.1365-2125.1994.tb04337.x.
We have evaluated the differential release of A, B and C-type natriuretic peptides in response to incremental doses of angiotensin II (2, 4 and 6 ng kg-1 min-1). Baseline plasma concentrations of ANP (5.99 +/- 0.74 pmol 1-1) were significantly (P < 0.05) higher than BNP (1.53 +/- 0.48 pmol 1-1) or CNP (0.41 +/- 0.11 pmol 1-1). Angiotensin II infusion caused a significant (P < 0.05) increase in plasma ANP to 53.76 +/- 17.3 pmol 1-1 at 6 ng kg-1 min-1. Plasma concentrations of BNP and CNP were not significantly affected by angiotensin II. Arterial blood pressures and systemic vascular resistance increased (P < 0.001) in response to angiotensin II infusion. Thus, ANP, unlike BNP or CNP, is released acutely in response to the pressor stimulus of angiotensin II. This may represent a dissociation in release of the natriuretic peptides, in terms of short and long term responses to activation of the renin-angiotensin system.
我们评估了A、B和C型利钠肽对递增剂量血管紧张素II（2、4和6 ng kg-1 min-1）的差异释放情况。心房钠尿肽（ANP）的基线血浆浓度（5.99±0.74 pmol 1-1）显著高于脑钠肽（BNP，1.53±0.48 pmol 1-1）或C型利钠肽（CNP，0.41±0.11 pmol 1-1）（P<0.05）。输注血管紧张素II导致血浆ANP在6 ng kg-1 min-1时显著升高（P<0.05）至53.76±17.3 pmol 1-1。血管紧张素II对BNP和CNP的血浆浓度无显著影响。输注血管紧张素II后动脉血压和全身血管阻力升高（P<0.001）。因此，与BNP或CNP不同，ANP会对血管紧张素II的升压刺激产生急性释放。就肾素-血管紧张素系统激活的短期和长期反应而言，这可能代表利钠肽释放的分离。
