Seino M, Abe K, Nushiro N, Yoshinaga K
Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Hypertension. 1988 Jan;11(1):34-40. doi: 10.1161/01.hyp.11.1.34.
We examined a possible interaction between the calcium entry blocker nifedipine and atrial natriuretic peptide on blood pressure and natriuresis in anesthetized rabbits. The administration of atrial natriuretic peptide (0.05 micrograms/kg/min) produced a significant decrease in mean arterial pressure. Similar reductions in blood pressure were obtained during the administration of nifedipine (1.0 micrograms/kg/min). Atrial natriuretic peptide produced a consistent increase in glomerular filtration rate that was higher than the increase in renal blood flow; hence, the filtration fraction was significantly elevated. Atrial natriuretic peptide also elicited a significant increment in urine volume and urinary sodium excretion, while nifedipine was devoid of any significant effects on renal hemodynamics and renal excretory function during the experimental period. The administration of atrial natriuretic peptide superimposed on an ongoing infusion of nifedipine resulted in a greater fall of blood pressure than that seen during the administration of atrial natriuretic peptide or nifedipine alone. Sodium excretion was also potentiated, but there were no changes in renal hemodynamics or in the filtration fraction. These results suggest that calcium entry blockers potentiate the vasodepressor and the natriuretic effects of atrial natriuretic peptide but prevent its renal hemodynamic effects.
我们研究了钙通道阻滞剂硝苯地平与心房利钠肽对麻醉兔血压和利钠作用之间可能存在的相互作用。给予心房利钠肽(0.05微克/千克/分钟)可使平均动脉压显著降低。给予硝苯地平(1.0微克/千克/分钟)期间也出现了类似的血压降低。心房利钠肽使肾小球滤过率持续增加,且高于肾血流量的增加;因此,滤过分数显著升高。心房利钠肽还引起尿量和尿钠排泄显著增加,而在实验期间硝苯地平对肾血流动力学和肾排泄功能无任何显著影响。在持续输注硝苯地平的基础上给予心房利钠肽,导致血压下降幅度大于单独给予心房利钠肽或硝苯地平。钠排泄也增强,但肾血流动力学或滤过分数无变化。这些结果表明,钙通道阻滞剂可增强心房利钠肽的血管舒张和利钠作用,但可防止其对肾血流动力学的影响。