Seino M, Abe K, Nushiro N, Omata K, Itoh S, Yoshinaga K
Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Agents Actions Suppl. 1987;22:239-46. doi: 10.1007/978-3-0348-9299-5_25.
To examine whether hemodynamic and natriuretic effects of alpha-human atrial natriuretic peptide (ANP) were modulated by calcium (Ca) ion, Ca entry blocker nifedipine (Nif) was administered prior to ANP infusion in anesthetized rabbits. We also examined the effect of Nif and ANP on the renal kallikrein-kinin system. Both Nif. (1.0 micrograms/kg/min) and ANP (50 ng/kg/min) increased urinary sodium excretion (UNaV) without change in renal hemodynamics, although mean arterial pressure (MAP) decreased. Fractional excretion of sodium (FENa) was also increased significantly by both Nif and ANP. Nif infusion alone decreased MAP, the additional infusion of ANP on Nif pretreatment induced a further decrease in MAP and caused an increase in UNaV and FENa without renal hemodynamics changes. The administration of ANP increased urinary excretion of kallikrein and kinin. The additional infusion of ANP on Nif pretreatment induced a further increase in urinary kallikrein and kinin. These results suggest that Ca ion does not participate in ANP-induced natriuresis. Renal kallikrein-kinin may partly involve in natriuresis induced by ANP.
为研究钙离子是否调节α-人心房利钠肽(ANP)的血流动力学和利钠作用,在麻醉兔中于输注ANP前给予钙通道阻滞剂硝苯地平(Nif)。我们还研究了Nif和ANP对肾激肽释放酶-激肽系统的影响。Nif(1.0微克/千克/分钟)和ANP(50纳克/千克/分钟)均增加尿钠排泄(UNaV),且肾血流动力学无变化,尽管平均动脉压(MAP)降低。Nif和ANP均显著增加钠分数排泄(FENa)。单独输注Nif降低MAP,在Nif预处理基础上额外输注ANP导致MAP进一步降低,并使UNaV和FENa增加,而肾血流动力学无变化。给予ANP增加激肽释放酶和激肽的尿排泄。在Nif预处理基础上额外输注ANP导致尿激肽释放酶和激肽进一步增加。这些结果提示钙离子不参与ANP诱导的利钠作用。肾激肽释放酶-激肽可能部分参与ANP诱导的利钠作用。