Rubiales de Barioglio S, Lacuara J L, Graña M G
Instituto de Fisiología, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Argentina.
Acta Physiol Pharmacol Latinoam. 1988;38(1):69-75.
The present study investigates the effects of Sodium Nitroprusside (SNP) on isometric developed tension (IDT) and tonic component of K+ induced contracture of rat portal vein. The availability of activator calcium for the contraction was modified by changing the ionic composition of the Krebs Ringer bicarbonate medium (KRB) or by using pharmacological agents such as nifedipine or KCl. In control conditions (KRB media) magnitude of IDT was 10.61 +/- 0.56 mN (n = 13). Addition of increasing concentrations of SNP (non cumulative) diminished IDT in a dose related manner. Tonic component of 60 mM KCl evoked contracture decayed 27.04 +/- 10.9% (n = 6) after 10(-4)M SNP incubation. Relaxant effect of SNP was more pronounced in the presence of nifedipine 10(-10)M (72.35 +/- 7.5% of inhibition, n = 6). The sensitivity of the preparation to SNP was strongly reduced in conditions of diminished Ca+2 efflux (slow sodium media = KRB sucrose). Experiments here presented support the hypothesis that the vasodilator effect of SNP could be attributed to an enhanced Ca+2 efflux from the vessel.
本研究探讨硝普钠(SNP)对大鼠门静脉等长收缩张力(IDT)和钾离子诱导挛缩的强直成分的影响。通过改变 Krebs 林格碳酸氢盐培养基(KRB)的离子组成,或使用硝苯地平或氯化钾等药物,来改变收缩时激活钙的可用性。在对照条件下(KRB 培养基),IDT 的大小为 10.61±0.56 mN(n = 13)。添加递增浓度的 SNP(非累积)以剂量相关的方式降低了 IDT。在 10^(-4)M SNP 孵育后,60 mM 氯化钾诱发挛缩的强直成分衰减了 27.04±10.9%(n = 6)。在存在 10^(-10)M 硝苯地平的情况下,SNP 的舒张作用更为明显(抑制率为 72.35±7.5%,n = 6)。在钙离子外流减少的条件下(慢钠培养基 = KRB 蔗糖),制剂对 SNP 的敏感性大大降低。此处呈现的实验支持以下假设:SNP 的血管舒张作用可能归因于血管中钙离子外流的增强。